CA2567621A1 - Herbal product comprising cinnamon, bitter melon and omega-3 fatty acids - Google Patents
Herbal product comprising cinnamon, bitter melon and omega-3 fatty acids Download PDFInfo
- Publication number
- CA2567621A1 CA2567621A1 CA002567621A CA2567621A CA2567621A1 CA 2567621 A1 CA2567621 A1 CA 2567621A1 CA 002567621 A CA002567621 A CA 002567621A CA 2567621 A CA2567621 A CA 2567621A CA 2567621 A1 CA2567621 A1 CA 2567621A1
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- therapeutic formulation
- chocolate
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Abstract
This invention relates to a new herbal product comprising cinnamon (Cinnamomi cassiae: Cinnamonum verum) and bitter melon (Momordica charantia) and omega-3 fatty acids and, optionally, chocolate. Each of these ingredients is known to demonstrate therapeutic effects but the combination of the three ingredients demonstrates significant synergism and improved therapeutic effects.
Description
Title HERBAL PRODUCT COMPRISING CINNAMON, BITTER MELON
Field of the Invention 100011 This invention relates to a new herbal product and in particular, to a new herbal product comprising cinnamon (Cinnamomi cassiae: Cinnamonum verum) and bitter melon (Momordica charantia). Each of these ingredients is known to demonstrate therapeutic effects but the combination of the two ingredients demonstrates significant synergism and improved therapeutic effects.
Background of the Invention [0002] Diabetes, hyperlipidemis and obesity, besides being detrimental to health by themselves, are all recognized risk factors for cardiovascular disease (CVD), which is still the number one killer in North America. Obesity is reaching epidemic proportions in N. America and Type 2 diabetes, with its close links to obesity, has become a major cause for concern. High blood cholesterol levels have persisted as a key factor in the development of atherosclerosis and CVD, and high triglycerides have also been recognized as an important risk factor, especially for women. The incidence of metabolic syndrome (also known as insulin resistance syndrome, or syndrome X), which presents as a cluster of characteristics and symptoms, including obesity, increased waist circumference, borderline high blood glucose and blood pressure levels, and abnormal blood lipid levels, has been increasing sharply since it was first recognised as a common precursor to both CVD and diabetes.
Field of the Invention 100011 This invention relates to a new herbal product and in particular, to a new herbal product comprising cinnamon (Cinnamomi cassiae: Cinnamonum verum) and bitter melon (Momordica charantia). Each of these ingredients is known to demonstrate therapeutic effects but the combination of the two ingredients demonstrates significant synergism and improved therapeutic effects.
Background of the Invention [0002] Diabetes, hyperlipidemis and obesity, besides being detrimental to health by themselves, are all recognized risk factors for cardiovascular disease (CVD), which is still the number one killer in North America. Obesity is reaching epidemic proportions in N. America and Type 2 diabetes, with its close links to obesity, has become a major cause for concern. High blood cholesterol levels have persisted as a key factor in the development of atherosclerosis and CVD, and high triglycerides have also been recognized as an important risk factor, especially for women. The incidence of metabolic syndrome (also known as insulin resistance syndrome, or syndrome X), which presents as a cluster of characteristics and symptoms, including obesity, increased waist circumference, borderline high blood glucose and blood pressure levels, and abnormal blood lipid levels, has been increasing sharply since it was first recognised as a common precursor to both CVD and diabetes.
[0003] While modern pharmaceutical drugs exist for the treatment of hyperlipidemia, diabetes, and CVD, the side effects associated with many of these drugs may have severely detrimental health effects which preclude their use, or these side effects may simply reduces patient compliance. As a result, a majority of the population has been looking elsewhere for the treatment of these diseases and conditions, and complementary therapies have become a popular alternative to the pharmaceutical model for treatment.
I
I
[0004] Two herbal products which are likely candidates as treatment options are bitter melon (Momordica charantia) and cinnamon (Cinnamomi cassiae; Cinnamomum verum).
Bitter melon has been used for its pharmaceutical properties since the 16th century, by residents of tropical areas of the world. It has recognized anti-viral, anti-bacterial, anti-cancer, and immunomodulatory properties; however, in recent years, most research focus has been on the glucose-lowering ability of bitter melon. In animal studies, bitter melon supplementation of the diets of diabetic animals has resulted in improved oral glucose tolerance, a reduction in blood glucose levels and reduced insulin resistance. Furthermore, bitter melon has been observed to decrease obesity, and modestly reduce cholesterol and triglyceride levels in animal species.
Bitter melon has been used for its pharmaceutical properties since the 16th century, by residents of tropical areas of the world. It has recognized anti-viral, anti-bacterial, anti-cancer, and immunomodulatory properties; however, in recent years, most research focus has been on the glucose-lowering ability of bitter melon. In animal studies, bitter melon supplementation of the diets of diabetic animals has resulted in improved oral glucose tolerance, a reduction in blood glucose levels and reduced insulin resistance. Furthermore, bitter melon has been observed to decrease obesity, and modestly reduce cholesterol and triglyceride levels in animal species.
[0005] Like bitter melon, cinnamon has been widely used for centuries, and is a traditional folk herb for diabetes mellitus in Russia, China and Korea. It is also thought to possess anti-fever and antibiotic properties, as well as being as mild analgesic and sedative. Again, like bitter melon, recent research has focused on its ability to lower blood glucose levels. In recent animal studies, its blood-glucose-lowering ability was dose-dependent, with higher doses lowering glucose levels more than lower doses. Insulin levels increased, as did HDL
cholesterol levels (the so-called "good" cholesterol). Total and LDL cholesterol levels and triglyceride levels, on the other hand, were reduced with cinnamon supplementation. An additional benefit of cinnamon supplementation may be its antioxidant capacity, due to its phenolic acids and flavonoids. This antioxidant capacity may not only slow the progression of Type 2 diabetes complications, by quenching the excessive oxygen free radical damage seen in diabetes, it may also protect LDL cholesterol from oxidation, reducing the likelihood of it being scavenged and incorporated into blood vessel wall plaque, the latter being a major part of atherosclerosis, hypertension and CVD.
cholesterol levels (the so-called "good" cholesterol). Total and LDL cholesterol levels and triglyceride levels, on the other hand, were reduced with cinnamon supplementation. An additional benefit of cinnamon supplementation may be its antioxidant capacity, due to its phenolic acids and flavonoids. This antioxidant capacity may not only slow the progression of Type 2 diabetes complications, by quenching the excessive oxygen free radical damage seen in diabetes, it may also protect LDL cholesterol from oxidation, reducing the likelihood of it being scavenged and incorporated into blood vessel wall plaque, the latter being a major part of atherosclerosis, hypertension and CVD.
[0006] Thus far, human studies on either herb separately is extremely limited.
In animals, although bitter melon and cinnamon have similar physiological effects - lower blood glucose, cholesterol and triglyceride levels - their mechanisms of action are different.
In animals, although bitter melon and cinnamon have similar physiological effects - lower blood glucose, cholesterol and triglyceride levels - their mechanisms of action are different.
[0007] Accordingly, the present inventors have combined these two basic ingredients into a single therapeutic formulation which demonstrates synergistic results. The inventors have found that the new therapeutic formulation has resulted in the following:
1. Reduction in blood glucose levels and increased glucose tolerance in diabetics and people with metabolic syndrome.
2. Reduction in total and LDL cholesterol and triglycerides, and increase in HDL cholesterol in people with dyslipidemia, including people with metabolic syndrome.
3. Reduction in obesity.
4. Improved antioxidant capacity, with the potential to protect diabetics against free radical damage, and to reduce oxidized LDL cholesterol levels.
1. Reduction in blood glucose levels and increased glucose tolerance in diabetics and people with metabolic syndrome.
2. Reduction in total and LDL cholesterol and triglycerides, and increase in HDL cholesterol in people with dyslipidemia, including people with metabolic syndrome.
3. Reduction in obesity.
4. Improved antioxidant capacity, with the potential to protect diabetics against free radical damage, and to reduce oxidized LDL cholesterol levels.
[0008] Thus, this new therapeutic formulation may be used to treat diabetes and CVD, and also in the precursor syndrome, where almost all of the characteristics of this syndrome - high total and LDL cholesterol, high triglyceride, low HDL cholesterol, borderline high blood glucose levels, obesity and high waist circumference - may be improved. Even borderline high blood pressure, which is normally affected by the degree of obesity, may be reduced.
In effect, this therapeutic formulation will reduce the incidence of metabolic syndrome, which, in turn, would reduce the incidence of diabetes, CVD and obesity. This is the first herbal combination with the potential to have more significant effects than pharmaceutical drugs on this triumvirate of conditions which continues to have a major impact on the health of North Americans.
Summary of the Invention [0009] To this end, in one of its aspects, the present invention provides a novel therapeutic formulation which comprises cinnamon and bitter melon.
In effect, this therapeutic formulation will reduce the incidence of metabolic syndrome, which, in turn, would reduce the incidence of diabetes, CVD and obesity. This is the first herbal combination with the potential to have more significant effects than pharmaceutical drugs on this triumvirate of conditions which continues to have a major impact on the health of North Americans.
Summary of the Invention [0009] To this end, in one of its aspects, the present invention provides a novel therapeutic formulation which comprises cinnamon and bitter melon.
[0010] A further object of the present invention is to provide a new therapeutic formulation which comprises cinnamon and bitter melon in a ratio of seventy: thirty (70:30).
Detailed Description of the Invention [00011] The two active ingredients of the new therapeutic formulation are cinnamon and bitter melon. Both the plants are known to have hypoglycaemic properties in traditional Chinese, Indian and Caribbean Medicine.
Detailed Description of the Invention [00011] The two active ingredients of the new therapeutic formulation are cinnamon and bitter melon. Both the plants are known to have hypoglycaemic properties in traditional Chinese, Indian and Caribbean Medicine.
[00012] In recent years numerous laboratory and clinical studies have been conducted on these two plants by biological scientists, pharmacologists and pharmacists at prestigious research centres like Department of Pharmacy at the Kings College of London, University of California, Santa Barbara, Iowa State University and the U.S. Department of Agriculture.
All of these studies sliow findings that confirm the therapeutic properties of the plants claimed by the traditional medicine and some of the research actually is considered to be break through in the field of natural health products. At USDA, scientists have been able to identify the particular molecule in cinnamon that mimics insulin and is responsible for its hypoglycaemic properties.
All of these studies sliow findings that confirm the therapeutic properties of the plants claimed by the traditional medicine and some of the research actually is considered to be break through in the field of natural health products. At USDA, scientists have been able to identify the particular molecule in cinnamon that mimics insulin and is responsible for its hypoglycaemic properties.
[00013] The new therapeutic formulation contains cinnamon and bitter melon at a ratio of 70:30 which is the most synergistic combination of the two plants for the management of blood sugar levels of type 2 diabetes patients as well as for normalizing the lipid profiles.
[00014] The dietary habits of the developed countries such as Canada and United States have recently been criticized for causing an increase in the incidence of several types of lifestyle-related diseases such as diabetes, obesity and cardiovascular diseases.
Diabetes, a disorder of carbohydrate, fat and protein metabolism attributed to diminished production of insulin or mounting resistance to its action, is the most common metabolic disease presently. It is a major cause of disability and hospitalization resulting in a significant financial burden on the health care system (Rathi et al. 2002 and Virdi et al. 2003), and is estimated to cost Canadians up to $9 billion annually (Public Health Agency of Canada, 2005). It also has a significant impact on the health, quality of life and life expectancy of patients. Diabetes is a potent risk factor for cardiovascular disease as it not only affecting glucose metabolism but also influences lipid metabolism (Jayasooriya et al. 2000). Diabetes is divided into two major categories: type 1 diabetes, previously known as insulin dependent diabetes mellitus (IDDM), and type 2 diabetes, previously known as non-insulin dependent diabetes mellitus (NIDDM). Although the recommended treatments for these two categories are usually somewhat different, insulin for IDDM and lifestyle management for NIDDM, the overall result is improving glucose homeostasis. Lifestyle management such as changes in diet and an exercise regimen continues to be essential and effective but it may be insufficient or difficult for patient compliance rendering conventional drug therapies useful (Dey et al. 2002). The problems with the use of insulin or any other antidiabetic drugs are the presence of adverse effects such as hypoglycemia at higher doses, liver problems, lactic acidosis and diarrhea (Virdi et al.
2003). In recent years, there has been a growing interest in herbal medicines specifically herbal extracts as a popular alternative in healthcare due to people's perception of it being a'natural' product and therefore a minimal chance of having any side effects. The current popularity is also due to the many botanicals reported for the management of diabetes in other alternative systems of medicine such as Ayurveda and Traditional Chinese Medicine, the interest in these herbal plants has been piqued.
Diabetes, a disorder of carbohydrate, fat and protein metabolism attributed to diminished production of insulin or mounting resistance to its action, is the most common metabolic disease presently. It is a major cause of disability and hospitalization resulting in a significant financial burden on the health care system (Rathi et al. 2002 and Virdi et al. 2003), and is estimated to cost Canadians up to $9 billion annually (Public Health Agency of Canada, 2005). It also has a significant impact on the health, quality of life and life expectancy of patients. Diabetes is a potent risk factor for cardiovascular disease as it not only affecting glucose metabolism but also influences lipid metabolism (Jayasooriya et al. 2000). Diabetes is divided into two major categories: type 1 diabetes, previously known as insulin dependent diabetes mellitus (IDDM), and type 2 diabetes, previously known as non-insulin dependent diabetes mellitus (NIDDM). Although the recommended treatments for these two categories are usually somewhat different, insulin for IDDM and lifestyle management for NIDDM, the overall result is improving glucose homeostasis. Lifestyle management such as changes in diet and an exercise regimen continues to be essential and effective but it may be insufficient or difficult for patient compliance rendering conventional drug therapies useful (Dey et al. 2002). The problems with the use of insulin or any other antidiabetic drugs are the presence of adverse effects such as hypoglycemia at higher doses, liver problems, lactic acidosis and diarrhea (Virdi et al.
2003). In recent years, there has been a growing interest in herbal medicines specifically herbal extracts as a popular alternative in healthcare due to people's perception of it being a'natural' product and therefore a minimal chance of having any side effects. The current popularity is also due to the many botanicals reported for the management of diabetes in other alternative systems of medicine such as Ayurveda and Traditional Chinese Medicine, the interest in these herbal plants has been piqued.
[00015] The following is a brief description of the two ingredients and their therapeutic properties.
[00016] Cinnamomum aromaticum (sp. Cassia) is from the family Lauraceae. It is a medium-sized evergreen tree native to China and Vietnam. It contains volatile oils composed of cinnamaldehyde, phenolic compounds, flavonoid derivates, methylhydroxychalcone polymer, mucilage, calcium oxalate, resins, sugars, and coumarins. Cassia, the species name for Cinnamoinum aromaticum comes from the Greek work "kassia" meaning "to strip off the bark".
Cinnamon bark has been used medicinally in China since 2700 B.C.E and is said to supplement vital energy and blood, tone the kidney and spleen and acts as an antioxidant (Blumenthal et al.
1998). Cinnaniomum aromaticum has also been used in Korea, China and Russia as a traditional folk herb with hypoglycemic properties for the treatment of diabetes mellitus (Kim et al. 2005).
The increasing prevalence of diabetes and cardiovascular disease is evident worldwide with an estimated 1700 new cases diagnosed daily (Jarvill-Taylor et al. 2001).
Additionally, several million people worldwide are suffering from 'pre-diabetes' caused by high glucose levels with a resistance to insulin (Khan et al. 2003). The primary function of insulin is to maintain low blood glucose, lipid and cholesterol levels to maintain a sense of well-being.
Environmental factors such as diet, exercise, and stress also attribute to decreasing insulin sensitivity and increasing glucose and low-density lipoprotein (LDL) cholesterol levels, increasing the risk of cardiovascular diseases, obesity, dyslipidemias, diabetes mellitus and premature aging. The increase in disease is partly due to the augmented intake of calories and refined carbohydrates, lesser consumption of fibers and a more sedentary lifestyle. Controlling dietary intake and exercise could prevent disease but the majority of individuals require an extra aid to maintain normal health (Talpur et al., 2005). There is a growing interest in herbal remedies due to the side effects associated with therapeutic hypoglycemic agents and insulin (Kim et al. 2005).
Botanical products with a long history of safety are widely used to lower glucose, lipid and cholesterol levels and for the prevention and treatment of diabetes.
[000171 Cinnamomum aromaticum has been used as a hypoglycemic agent in ancient medicines (Kim et al. 2005). The modem therapeutic properties of cinnamon are supportable based on thousands of years of use in well established systems of traditional medicines, as well as some modem clinical studies (Blumenthal et al. 1998). A number of well proven in vivo animal studies on Cinnamomum aromaticum demonstrate that activation of the insulin receptor increases autophosphorylation resulting in an increase in glucose uptake and glycogen synthesis.
However, there is a limited amount of published data on the effects of cinnamon consumption on blood glucose in humans. In vivo, in vitro and human studies have established that cinnamon extract regulates insulin activity and reduces serum glucose and cholesterol levels (Khan et al.
2003 and Kim et al. 2005).
[00018] In a study by Khan et al. in 2003, 60 men and women with type 2 diabetes ingested daily doses of cinnamon or placebo capsules for 40 days followed by a 20-day washout period. Cinnamon capsules contained 1, 3 or 6 g of Cinnamomum aromaticum.
After 20 days, only the 6 g cinnamon group showed significantly lower glucose levels.
However, after 40 days, serum glucose (18-29%), triglycerides (23-30%) and total cholesterol (12-26%) concentrations were significantly lower in all cinnamon groups. Total cholesterol was lower in all groups at 40 days but low-density lipoprotein (LDL) concentrations were only significantly lower in the 3 g and 6 g cinnamon groups (10% and 24%, respectively). For the 1 g cinnamon group, LDL
concentrations continued to decline during the washout period and were significant at 60 days (P<0.05). The decreased concentration of glucose was maintained by the 1 g cinnamon group while triglyceride and total cholesterol levels were maintained in all cinnamon groups throughout the 20-day washout period.
[00019] Vanschoonbeek et al. 2006 performed a 6 week standardized placebo-controlled study to investigate the proposed benefits of Cinnamomum cassia on 25 postmenopausal women diagnosed with type 2 diabetes. Patients were divided into two groups and supplemented with 1.5 g/day of Cinnamomum or placebo to assess the effects on glucose tolerance and whole-body insulin sensitivity. At 0, 2 and 6 weeks oral glucose tolerance tests and blood lipid profiles were performed resulting in no time x treatment interaction observed for fasting glucose, insulin concentration, insulin resistance, (oral glucose) insulin sensitivity or fasting blood lipid concentrations. This study shows cinnamon supplementation does not have a health benefit in patients with type 2 diabetes contradicting the results found by Khan et al.
2003. Differences between the two studies could be attributed to the selection of patients and the combination of medications taken. In the current study, only postmenopausal female patients were included and continued using commonly prescribed combinations of oral blood glucose-lowering agents, which was not a factor in the study by Khan et al. 2003, explaining the low baseline values found in the patients used in the current study. Although the authors concluded cinnamon supplementation in combination with oral blood glucose-lowering agents may not be beneficial to overweight, postmenopausal women, this is a small concentrated study not factoring in the use of other medications and patient characteristics.
[000201 In a study by Talpur et al. in 2005, Zucker fatty rats (ZFRs) and spontaneously hyper-tensive rats (SHRs) were fed water or essential oils in acute or chronic doses to assess the effect of essential oil combinations on insulin sensitivity. The essential oil treatment consisted of 8 essential oils including cinnamon. Insulin sensitivity was determined by systolic blood pressure (SBP) and a glucose tolerance test. In the acute study, ZFRs and SHRs with essential oil treatments showed significant decreases in SBP at 4, 10 and 20 hours and at 4 hours, respectively. However, SBP levels were equal to the control group at 30 hours in ZFRs and at 10, 20 and 30 hours in SHRs. In the chronic study, ZFRs and SHRs consuming the essential oils showed significantly lower SBP at 8, 17 and 25 days in comparison to the control group.
Decreases in SBP levels ranged from 11 to 20 mmHg. During the oral glucose test, ZFRs consuming the essential oil combination showed consistently lower levels of circulating insulin, however these results were not significant. SHRs did not produce any effect on insulin levels and were equal to the controls, paralleling previous studies where effects were only produced when rats were challenged in stress-free environments (Verspohl et al. 2005).
The decreases in SBP and circulating glucose levels, produced by both species of rats, enhance insulin sensitivity and parallels the idea that fluctuating SBP is the most sensitive index of insulin sensitivity.
Cinnamon has been shown to have insulin-like actions and affect insulin signaling (Broadhurst et al. 2000), and as an ingredient in the essential oil combination it may have a role in the reduction of SBP.
[00021] In another study, Kim et al. 2006, administered db/db mice Cinnamomum cassia dosages of 50, 1.00, 150 or 200 mg/kg for 6 weeks to determine its effect on blood glucose. The control group showed high blood glucose levels at 2, 4, and 6 weeks. The cinnamon extract-treated group showed significantly lower blood glucose levels at each time period (P<0.05, <0.01 and <0.001). Significant decreases in triglyceride and total cholesterol levels were noted in the cinnamon extract group. Similar to Khan et al. 2003 these results parallel the hypoglycemic effects in the cinnamon extract-treated group as reduced levels are maintained for a long period of time.
1000221 In a similar study by Verspohl et al. in 2005, blood glucose and plasma insulin levels were evaluated in Wistar rats given extracts of Cinnamomum bark, cassia or zeylanicum.
During the glucose tolerance test, plasma insulin levels increased significantly after the administration of Cinnamomum extracts with cassia showing the most pronounced effect. The saline placebo group showed no effect on plasma insulin. In all extract-treated groups, blood glucose levels did not decrease unless the rat was challenged by a glucose tolerance test in a stress-free environment. Cinnamomum cassia produced a direct insulin stimulatory effect showing superior effects compared to zeylanicum.
[00023] The increase in fructose consumption has risen worldwide in the past two decades as a significant proportion of energy intake in the diet. Qin et al. 2004 fed 18 male Wistar rats a high-fructose diet and 6 a control diet for 3 weeks to determine the effects of glucose utilization and insulin sensitivity. 12 of the rats consuming a high-fructose diet had Cinnamomum cassia extracts (300 mg/kg/day) added to their diet. During the euglycemic clamp procedure to measure glucose infusion rates (GIR), the 6 rats consuming only a high-fructose diet showed significant decreases (p<0.0001) in glucose infusion rates while cinnamon treated rats produced significant increases, similar to the controls. The consumption of a high-fructose diet, an environmental factor contributing to diabetes, is common in the western society; the addition of Cinnamomum cassia extract to the diet shows a preventative effect, through an increase in glucose utilization and insulin sensitivity.
[000241 In another study, the effect of cinnamon extract on insulin action was evaluated in Wister rats. Qin et al. 2003 randomly assigned 18 rats into three groups:
saline, 30mg/kg and 300mg/kg cinnamon extract. Cinnamon treatment for 3 weeks did not have an effect on plasma free fatty acids and fasting blood glucose concentrations. Although these levels were not affected in the cinnamon treated group, a difference was prevalent in glucose uptake compared to the placebo group. A dose-dependent manner was noticed with glucose utilization as 300mg/kg enhanced glucose utilization to a greater degree than the 30mg/kg or control groups.
[00025] Methylhydroxychalcone polymer (MHCP), a bioactive compound of cinnamon extract, is hypothesized to trigger an insulin-like response. In a study by Jarvill-Taylor et al.
2001, 3T3-L1 adipocytes were assessed with MHCP to determine its function as an insulin mimetic. Within the first 10 minutes of incubation, the insulin treated adipocytes showed a 2.5 fold increase in glucose transport while the MHCP treated group did not show any increase.
However, gradually over the one-hour period, glucose uptake increased in the MHCP treated group and at 60 minutes, a significant increase was noted. As noted in other studies, the effect of cinnamon did not diminish immediately after stopping treatment. As MHCP is administered, the kinase receptor is activated resulting in phosphorylation of the insulin receptor, a similar effect is seen throughout the insulin signaling pathway.
[00026] A similar study by Broadhurst et al. in 2000 reported an increase in insulin action demonstrated by cinnamon extract in vitro. Rat epididymal adipocytes were given either insulin or cinnamon extract after incubation to determine glucose metabolism. At all dilutions (1:2, 1:10, 1:50) cells exposed to cinnamon extract showed a significant increase in insulin-dependent activity and the effect was maintained at the high dilution (1:50). As adipocytes were treated with cinnamon extract the insulin receptor kinase became activated, a necessary requirement to increase insulin sensitivity. The activation of kinase mimics insulin activity in adipocytes.
Afterwards, active cinnamon extract was incubated with soluble polyvinylpyrrolidone (PVP) to determine if activity was associated with tannins or polyphenols. Cinnamon readily bound to PVP giving it a polyphenolic characterization. With an increase in glucose metabolism, 98% of activity is attributed to PVP indicating the use of phenolics to destroy free radicals that inhibit the activation of insulin-receptor kinase. Cinnamon extract mimics the same mechanism as insulin in adipocytes, increasing insulin sensitivity and glucose metabolism.
[000271 Cinnamomum aromaticum (cinnamon) has convincingly been shown to prevent and control elevated glucose and blood lipid concentrations in both in vitro and in vivo studies and can be maintained for a long period after use. The insulin kinase receptor is activated with cinnamon extract demonstrating insulin-mimetic activity. Elevated glucose and blood lipid concentrations increase the incidence of diabetes and/or cardiovascular health. The use of cinnamon extract can prevent these diseases by regulating the insulin receptor to increase glucose uptake and metabolism.
[00028] To date there have been no formal pharmacokinetic studies done on this plant in animals or humans. The only information derived from literature was a study conducted by Khan et al. in 2003 that found Cinnamomum aromaticum (extract) has a prolonged effect on the human body for 20 days during the washout period. Several animal studies have also shown prolonged effects after consumption of cinnamon extract.
[00029] The exact mechanism of action of Cinnamomum aromaticum (extract) is thought to be that it acts as an insulin-mimetic by activating the kinase receptor and increasing insulin sensitivity. The interaction within the intracellular kinase domain triggers an insulin-like response and stimulates glucose oxidation. Cinnamon also regulates enzymes inside the insulin receptor kinase domain and inhibits both phosphotyrosine-specific protein phosphatase (PTP-1) in vitro and glycogen synthase kinase-3(3 (GSK-3(3) in vivo. The inhibition of PTP-1 keeps the insulin receptor in an activated state and inhibition of GSK-30 stimulates glycogen production.
Cinnamon acts independently from insulin but similar levels of activity were observed proposing that it may activate the same cascade as the insulin signaling pathways (Jarvill-Taylor et al.
2001).
1000301 Cinnamon significantly helps people with type 2 diabetes improve their ability to respond to insulin, thus normalizing their blood sugar levels. Both test tube and animal studies have shown that compounds in cinnamon not only stimulate insulin receptors, but also inhibit an enzyme that inactivates them, thus significantly increasing cells' ability to use glucose. Studies to confirm cinnamon's beneficial actions in humans are currently underway with the most recent report coming from researchers from the US Agricultural Research Service, who have shown that less than half a teaspoon per day of cinnamon reduces blood sugar levels in persons with type 2 diabetes. Their study included 60 Pakistani volunteers with type 2 diabetes who were not taking insulin. Subjects were divided into six groups. For 40 days, groups 1, 2 and 3 were given 1, 3, or 6 grams per day of cinnamon while groups 4, 5 and 6 received placebo capsules. Even the lowest amount of cinnamon, 1 gram per day (approximately '/4 to %2 teaspoon), produced an approximately 20% drop in blood sugar; cholesterol and triglycerides were lowered as well.
When daily cinnamon was stopped, blood sugar levels began to increase.
1000311 Test tube, animal and human studies have all recently investigated cinnamon's ability to improve insulin activity, and thus our cells' ability to absorb and use glucose from the blood.
[00032] Ongoing in vitro or test tube research conducted by Richard Anderson and his colleagues at the USDA Human Nutrition Research Center is providing new understanding of the mechanisnls through which cinnamon enhances insulin activity. In their latest paper, published in the Journal ofAgricultural and Food Chemistry, Anderson et al.
characterize the insulin-enhancing complexes in cinnamon-a collection of catechin/epicatechin oligomers that increase the body's insulin-dependent ability to use glucose roughly 20-fold..
Some scientists had been concerned about potentially toxic effects of regularly consuming cinnamon. This new research shows that the potentially toxic compounds in cinnamon bark are found primarily in the lipid (fat) soluble fractions and are present only at very low levels in water soluble cinnamon extracts, which are the ones with the insulin-enhancing compounds.
[00033] A recent animal study demonstrating cinnamon's beneficial effects on insulin activity appeared in the December 2003 issue of Diabetes Research and Clinical Practice. In this study, when rats were given a daily dose of cinnamon (300 mg per kilogram of body weight) for a 3 week period, their skeletal muscle was able to absorb 17% more blood sugar per minute compared to that of control rats, which had not received cinnamon, an increase researchers attributed to cinnamon's enhancement of the muscle cells' insulin-signaling pathway. In humans with type 2 diabetes, consuming as little as 1 gram of cinnamon per day was found to reduce blood sugar, triglycerides, LDL (bad) cholesterol, and total cholesterol, in a study published in the December 2003 issue of Diabetes Care. The placebo-controlled study evaluated 60 people with type 2 diabetes (30 men and 30 women ranging in age from 44 to 58 years) who were divided into 6 groups. Groups 1, 2, and 3 were given 1, 3, or 6 grams of cinnamon daily, while groups 4, 5, and 6 received 1, 3 or 6 grams of placebo. After 40 days, all three levels of cinnamon reduced blood sugar levels by 18-29%, triglycerides 23-30%, LDL
cholesterol 7-27%, and total cholesterol 12-26%, while no significant changes were seen in those groups receiving placebo. The researchers' conclusion: including cinnamon in the diet of people with type 2 diabetes will reduce risk factors associated with diabetes and cardiovascular diseases.(January 28, 2004) 1000341 The latest research on cinnamon shows that by enhancing insulin signaling, cinnamon can prevent insulin resistance even in animals fed a high-fructose diet! A study published in the February 2004 issue of Hormone Metabolism Research showed that when rats fed a high-fructose diet were also given cinnamon extract, their ability to respond to and utilize glucose (blood sugar) was improved so much that it was the same as that of rats on a normal (control) diet. Cinnamon is so powerful an antioxidant that, when compared to six other antioxidant spices (anise, ginger, licorice, mint, nutmeg and vanilla) and the chemical food preservatives (BHA (butylated hydroxyanisole), BHT (butylated hydroxytoluene), and propyl gallate), cinnamon prevented oxidation more effectively than all the other spices (except mint) and the chemical antioxidants. (May 6, 2004).
[00035] In addition to its unique essential oils, cinnamon is an excellent source of the trace mineral manganese and a very good source of dietary fiber, iron and calcium.
The combination of calcium and fiber in cinnamon is important and can be helpful for the prevention of several different conditions. Both calcium and fiber can bind to bile salts and help remove them from the body. By removing bile, fiber helps to prevent the damage that certain bile salts can cause to colon cells, thereby reducing the risk of colon cancer. In addition, when bile is removed by fiber, the body must break down cholesterol in order to make new bile. This process can help to lower high cholesterol levels, which can be helpful in preventing atherosclerosis and heart disease.
[00036] Cinnamaldehyde (also called cinnamic aldehyde) has been well-researched for its effects on blood platelets. Platelets are constituents of blood that are meant to clump together under emergency circumstances (like physical injury) as a way to stop bleeding, but under normal circumstances, they can make blood flow inadequate if they clump together too much.
The cinnaldehyde in cinnamon helps prevent unwanted clumping of blood platelets. (The way it accomplishes this health-protective act is by inhibiting the release of an inflammatory fatty acid called arachidonic acid from platelet membranes and reducing the formation of an inflammatory messaging molecule called thromboxane A2.) Cinnamon's ability to lower the release of arachidonic acid from cell membranes also puts it in the category of an "anti-inflammatory" food that can be helpful in lessening inflammation.
[00037] Cinnamon's essential oils also qualify it as an "anti-microbial" food, and cinnamon has been studied for its ability to help stop the growth of bacteria as well as fungi, including the commonly problematic yeast Candida. In laboratory tests, growth of yeasts that were resistant to the commonly used anti-fungal medication fluconazole was often (though not always) stopped by cinnamon extracts.
[00038] Cinnamon's antimicrobial properties are so effective that recent research demonstrates this spice can be used as an alternative to traditional food preservatives. In a study, published in the August 2003 issue of the International Journal of Food Microbiology, the addition of just a few drops of cinnamon essential oil to 100 ml (approximately 3 ounces) of carrot broth, which was then refrigerated, inhibited the growth of the food borne pathogenic Bacillus cereus for at least 60 days. When the broth was refrigerated without the addition of cinnamon oil, the pathogenic B. cereus flourished despite the cold temperature. In addition, researchers noted that the addition of cinnamon not only acted as an effective preservative but improved the flavor of the broth.(October 1, 2003) [00039] In addition to the active components in its essential oils and its nutrient composition, cinnamon has also been valued in energy-based medical systems, such as Traditional Chinese Medicine, for its warming qualities. In these traditions, cinnamon has been used to provide relief when faced with the onset of a cold or flu, especially when mixed in a tea with some fresh ginger.
1000401 Bitter melon is of the family Cucurbitaceae, genus Momordica and species charantia. Some synonyms include Momordica chinensis, M. elegans, M. indica, M. operculata, M. sinensis, Sicyosfauriei, and its common names are bitter melon, papailla, melao de sao caetano, bittergourd, balsam apple, balsam pear, karela, k'u kua kurela, kor-kuey, ku gua, pava-aki, salsamino, sorci, sorossi, sorossie, sorossies, pare, peria laut, peria.
It may be used as a whole plant, fruit or seed.
[00041] Bitter melon grows in tropical areas, including parts of the Amazon, east Africa, Asia, and the Caribbean, and is cultivated throughout South America as a food and medicine. It's a slender, climbing annual vine with long-stalked leaves and yellow, solitary male and feniale flowers borne in the leaf axils. The fruit looks like a warty gourd, usually oblong and resembling a small cucumber. The young fruit is emerald green, turning to orange-yellow when ripe. At maturity, the fruit splits into three irregular valves that curl backwards and release numerous reddish-brown or white seeds encased in scarlet arils. The Latin name Momordica means "to bite," referring to the jagged edges of the leaves, which appear as if they have been bitten. All parts of the plant, including the fruit, taste very bitter.
1000421 In the Amazon, local people and indigenous tribes grow bitter melon in their gardens for food and medicine. They add the fruit and/or leaves to beans and soup for a bitter or sour flavor; parboiling it first with a dash of salt may remove some of the bitter taste.
Medicinally, the plant has a long history of use by the indigenous peoples of the Amazon. A leaf tea is used for diabetes, to expel intestinal gas, to promote menstruation, and as an antiviral for measles, hepatitis, and feverish conditions. It is used topically for sores, wounds, and infections and internally and externally for worms and parasites.
1000431 In Brazilian herbal medicine, bitter melon is used for tumors, wounds, rheumatism, malaria, vaginal discharge, inflammation, menstrual problems, diabetes, colic, fevers, worms. It is also used to induce abortions and as an aphrodisiac. It is prepared into a topical remedy for the skin to treat vaginitis, hemorrhoids, scabies, itchy rashes, eczema, leprosy and other skin problems. In Mexico, the entire plant is used for diabetes and dysentery; the root is a reputed aphrodisiac. In Peruvian herbal medicine, the leaf or aerial parts of the plant are used to treat measles, malaria, and all types of inflammation. In Nicaragua, the leaf is commonly used for stomach pain, diabetes, fevers, colds, coughs, headaches, malaria, skin complaints, menstrual disorders, aches and pains, hypertension, infections, and as an aid in childbirth.
[00044] Bitter melon contains an array of biologically active plant chemicals including triterpenes, proteins, and steroids. One chemical has clinically demonstrated the ability to inhibit the enzyme guanylate cyclase that is thought to be linked to the cause of psoriasis and also necessary for the growth of leukemia and cancer cells. In addition, a protein found in bitter melon, momordin, has clinically demonstrated anticancerous activity against Hodgkin's lymphoma in animals. Other proteins in the plant, alpha- and beta-momorcharin and cucurbitacin B, have been tested for possible anticancerous effects. A chemical analog of these bitter melon proteins has been developed and named "MAP-30"; its developers reported that it was able to inhibit prostate tumor growth. Two of these proteins-alpha- and beta-momorcharin-have also been reported to inhibit HIV virus in test tube studies. In one study, HIV-infected cells treated with alpha- and beta-momorcharin showed a nearly complete loss of viral antigen while healthy cells were largely unaffected. MAP-30 has been claimed to be "useful for treating tumors and HIV infections..." Another clinical study showed that MAP-30's antiviral activity was also relative to the herpes virus in vitro.
[00045] In numerous studies, at least three different groups of constituents found in all parts of bitter nielon have clinically demonstrated hypoglycemic (blood sugar lowering) properties or other actions of potential benefit against diabetes mellitus.
These chemicals that lower blood sugar include a mixture of steroidal saponins known as charantins, insulin-like peptides, and alkaloids. The hypoglycemic effect is more pronounced in the fruit of bitter melon where these chemicals are found in greater abundance.
1000461 Alkaloids, charantin, charine, cryptoxanthin, cucurbit, cucurbitaceous, cucurbitanes, cycloartenols, diosgenin, elaeostearic acids, erythrodiol, galacturonic acids, gentisic acid, goyaglycosides, goyasaponins, guanylate cyclase inhibitors, gypsogenin, hydroxytryptamines, karounidiols, lanosterol, lauric acid, linoleic acid, linolenic acid, momorcharasides, momorcharins, momordenol, momordicilin, momordicins, momordicinin, momordicosides, momordin, multiflorenol, myristic acid, nerolidol, oleanolic acid, oleic acid, oxalic acid, pentadecans, peptides, petroselinic acid, polypeptides, proteins, ribosome-inactivating proteins, rosmarinic acid, rubixanthin, spinasterol, steroidal glycosides, stigmasta-diols, stigmasterol, taraxerol, trehalose, trypsin inhibitors, uracil, vacine, v-insulin, verbascoside, vicine, zeatin, zeatin riboside, zeaxanthin, and zeinoxanthin are all found in bitter melon.
[00047] To date, close to 100 in vivo studies have demonstrated the blood sugar-lowering effect of this bitter fruit. The fruit has also shown the ability to enhance cells' uptake of glucose, to promote insulin release, and to potentiate the effect of insulin. In other in vivo studies, bitter melon fruit and/or seed has been shown to reduce total cholesterol. In one study, elevated cholesterol and triglyceride levels in diabetic rats were returned to normal after 10 weeks of treatment.
1000481 Several in vivo studies have demonstrated the antitumorous activity of the entire plant of bitter melon. In one study, a water extract blocked the growth of rat prostate carcinoma;
another study reported that a hot water extract of the entire plant inhibited the development of mammary tumors in mice. Numerous in vitro studies have also demonstrated the anticancerous and antileukemic activity of bitter melon against numerous cell lines, including liver cancer, human leukemia, melanoma, and solid sarcomas.
1000491 Bitter melon, like several of its isolated plant chemicals, also has been documented with in vitro antiviral activity against numerous viruses, including Epstein-Barr, herpes, and HIV viruses. In an in vivo study, a leaf extract increased resistance to viral infections and had an immunostimulant effect in humans and animals, increasing interferon production and natural killer cell activity.
[00050] In addition to these properties, leaf of bitter melon have demonstrated broad-spectrum antimicrobial activity. Various extracts of the leaves have demonstrated in vitro antibacterial activities against E. coli, Staphylococcus, Pseudomonas, Salmonella, Streptobacillus, and Streptococcus; an extract of the entire plant was shown to have antiprotozoal activity against Entamoeba histolytica. The fruit and fruit juice have demonstrated the same type of antibacterial properties and, in another study, a fruit extract demonstrated activity against the stomach ulcer-causing bacteria Helicobacterpylori.
1000511 Many in vivo clinical studies have demonstrated the relatively low toxicity of all parts of the bitter melon plant when ingested orally. However, toxicity and even death in laboratory animals has been reported when extracts are injected intravenously.
Other studies have shown extracts of the fruit and leaf (ingested orally) to be safe during pregnancy. The seeds, however, have demonstrated the ability to induce abortions in rats and mice, and the root has been documented as a uterine stimulant in animals. The fruit and leaf of bitter melon have demonstrated an in vivo antifertility effect in female animals; and in male animals, to affect the production of sperm negatively.
[00052] Over the years scientists have verified many of the traditional uses of this bitter plant that continues to be an important natural remedy in herbal medicine systems. Bitter melon capsules and tinctures are becoming more widely available in the United States and are employed by natural health practitioners for diabetes, viruses, colds and flu, cancer and tumors, high cholesterol, and psoriasis. Concentrated fruit and seed extracts can be found in capsules and tablets, as well as whole herb/vine powders and extracts in capsules and tinctures.
1000531 Bitter melon traditionally has been used as an abortive and has been documented with weak uterine stimulant activity; therefore, it is contraindicated during pregnancy.
[00054] This plant has been documented to reduce fertility in both males and females and should therefore not be used by those undergoing fertility treatment or seeking pregnancy.
1000551 The active chemicals in bitter melon can be transferred through breast milk;
therefore, it is contraindicated in women who are breast feeding.
[00056] All parts of bitter melon (especially the fruit and seed) have demonstrated in numerous in vivo studies that they lower blood sugar levels. As such, it is contraindicated in persons with hypoglycemia.
[00057] Although all parts of the plant have demonstrated active antibacterial activity, none have shown activity against fungi or yeast. Long-term use of this plant may result in the die-off of friendly bacteria with resulting opportunistic overgrowth of yeast (Candida). Cycling off the use of the plant (every 21-30 days for one week) may be warranted, and adding probiotics to the diet may be beneficial if this plant is used for longer than 30 days.
[00058] Bitter melon may potentiate insulin and anti-diabetic drugs and cholesterol-lowering drugs.
[00059] As stated before, Momordica charantia or commonly referred to as bitter melon has been one of the most extensively investigated and most widely acclaimed remedy for the treatment of diabetes since ancient time as all parts of the plant (fruit pulp, seed, leaves and whole plant) have shown hypoglycemic activity in normal animals, antihyperglycemic activity in alloxan or streptozotocin-induced diabetic animals and in genetic models of diabetes (Ahmed et al. 2001, Virdi et al. 2003 and Grover and Yadav 2004). Bitter melon has been observed to decrease serum glucose levels in animal experiments and in a few methodologically weak human studies as these investigations were neither randomized nor blinded and the dosage, toxicity and adverse effects have not been systematically assessed (Basch et al. 2003).
Nonetheless, the human, animal and in vitro evidence collectively suggests a moderate hypoglycemic effect of bitter melon.
[00060] A study by Akhtar et al. in 1981, investigated the effect of dried and powdered M.
charantia fruit on blood glucose level following oral administration to normal and alloxan-diabetic rabbits. Both normal and diabetic rabbits were randomly divided into 5 groups of six animals where group I served as a control whereas group II, III, IV and V were treated orally with 0.25, 0.5, 1.00 and 1.5 g/kg body weight of M. charantia powder suspended in 1%
carboxymethyl cellulose solution in water respectively. Blood was collected from an ear vein immediately after M. charantia administration at 5, 10 and 24 hour time intervals. There was no decrease in blood glucose at a dose of 0.25 g/kg in normal rabbits and at 0.25 and 0.5 g/kg in diabetic rabbits. The maximum glucose decrease was observed at 10 hours intervals in both normal and diabetic rabbits. A dose dependent decrease in blood glucose levels was observed at a dose of 1.0 and 1.5 g/kg in diabetic rabbits. The authors concluded that the whole dried powdered M. charantia fruit produced significant and consistent hypoglycemic effect in both normal and chemically induced insulin deficient rabbits.
[00061] In a study by Khanna et al. (1981), pharmacological trials on animals and clinical trials on humans were performed to investigate the effect of a hypoglycemic agent, polypeptide-p, isolated from the fruit, seeds and tissues of M. charantia. This active principle was actually isolated earlier by Khanna et al. in another study and was then called 'p-insulin' or 'v-insulin'.
The pharmacological trials in gerbils and langurs revealed that the polypeptide-p-ZnCIZ
administered subcutaneously was long acting and showed a significant blood-sugar-lowering effect. The clinical study also showed a hypoglycemic effect of polypeptide-p in juvenile and maturity-onset diabetic patients.
[00062] In a study by Leatherdale et al. (1981), the effect ofM. charantia on glucose and insulin concentrations was studied in non-insulin dependent diabetics and non-diabetic rats during a 50 g oral glucose tolerance test. Patients underwent three 50 g oral glucose tests: a standard test, a test with 50 mL ofjuice extracted from fresh M. charantia and a test after 8 - 11 weeks of consuming 0.23 kg of fried M. charantia daily. The rats were given 2 mL of the 10 mL
obtained from 100 g M. charantia. There was no associated increase in serum insulin response but blood glucose concentrations were significantly reduced in both patients and rats with the administration of raw juice whereas the daily supplement of fried M. charantia produced a small but significant improvement in glucose tolerance.
[00063] In a similar study by Welihinda et al. (1986), the hypoglycemic activity of M.
charantia was evaluated in non-insulin dependent maturity onset diabetics.
This study involved 18 patients with newly diagnosed type 2 diabetes mellitus. Each subject was given 100 mL of bitter melon juice 30 minutes before glucose loading for a glucose tolerance test (GTT). The results were compared to a GTT done on the previous day by each participant that showed significant improvements in GTT in 13 of the 18 participants (73%) after taking bitter melon.
The other 5 patients showed no significant improvements in their glucose tolerance. The authors explained that this may have been due to intra-individual variation which is normally seen in biological systems.
[00064] A study by Day et al. (1990), investigated the hypoglycemic effect of M.
charantia in normal mice by examining the plasma glucose and insulin responses to oral and intraperitoneal (i.p.) glucose tolerances and by examining different solvent-extracted fractions of M. charantia in streptozotocin diabetic mice. The hypoglycemic effect was evident at 60 minutes after oral glucose and 60 and 120 minutes after i.p. glucose at a dose of 1 g/mL. As in the experiment with the diabetic mice, oral administration of aqueous extract of M. charantia and residue after alkaline chloroform extraction reduced plasma glucose concentration within 1 hour also at a dose of lg/mL. Material recovered by acid water wash of the chloroform extract at a dose of 0.002g/mL produced a slowly generated hypoglycemic effect. Orally administered M.
charantia extracts lower glucose concentrations independently of intestinal glucose absorption and involves an extra-pancreatic action.
1000651 The hypoglycemic effects of fruit pulp, seed and whole plant of M.
charantia were studied in normal, IDDM and NIDDM model rats by Ali et al. in 1993.
Diabetes stimulating both IDDM and NIDDM were induced by i.p. injection of streptozotocin. The results indicated that the hypoglycemic principle is present only in the fruit pulp and that no blood glucose lowering effect was seen in either nonnal or diabetic (IDDM and NIDDM) rats when given seed extracts. It was noted that the fruit pulp extracts showed hypoglycemic activity in normal and NIDDM rats whereas no effect was produced in the IDDM model where 0 cells have been almost completely destroyed. An indication that the hypoglycemic effect of the active principle is probably mediated either by improving the insulin-secretory capacity of 0 cells or by improving the action of insulin 1000661 However, in a 2005 study by Sathishsekar and Subramanian, the conclusion of the study was that the administration of M. charantia seeds showed a hypoglycemic effect. The objective of the study was to examine the effect of aqueous extracts from seeds of two varieties of M. charantia on oxidative stress in plasma and the pancreas of streptozotocin-induced diabetic rats in comparison to a standard hypoglycemic drug, glibenclamide. Male albino rats of Wistar strain were divided into five groups of six animals in each group as follows:
normal control, diabetic control, diabetic treated with seed extract 1, diabetic treated with seed extract 2 and diabetic administered with glibenclamide. The duration of the experiment was 30 days and then the rats were sacrificed. The increase levels of blood glucose and decrease level of insulin in diabetic rats were normalized in M. charantia seed extract and glibenclamide treated diabetic rats. Also, the levels of thiobarbituric acid-reactive substances, lipid-hydroperoxides and reduced glutathione in both plasma and pancreas were significantly reversed to near normalcy after treatment. The levels of vitamin C and vitamin E in plasma and the activities of superoxide dismutase, catalase and glutathione peroxidase in pancreas were reversed to near normal levels and decreased activities respectively after M. charantia seed extract and glibenclamide treatment. Hence, controlling blood glucose level will thereby prevent the formation of free radicals or it may scavenge the reactive oxygen metabolites through various antioxidant compounds.
[00067] The antihyperglycemic effects of three extracts of fresh and dried whole M.
charantia fruit were studied by Virdi et al. in 2003 and compared to glibenclamide, a known synthetic drug. After 4 weeks of treatment at a dose of 20 mg/kg body weight, all three extract powders lowered blood glucose however the aqueous extract showed the maximum efficacy comparable to that of glibenclamide. This extract was further tested for nephrotoxicity, hepatotoxicity and biochemical parameters. No toxicity to liver and kidneys were shown based on histological and biochemical parameters. In conclusion, the aqueous extract powder of M.
charantia could be safely used in diabetic patients to control hyperglycemia and taken on a long term basis.
[00068] In 2001, Vikrant et al. carried out an experiment to study the effects of different doses of alcoholic and aqueous extracts of M. charantia on the metabolic parameters of fructose fed rats. Fructose feeding led to insulin resistance-hyperinsulinemia, hyperglycemia and slight elevation in serum triglycerides levels in which only aqueous extracts at the dose of 400 mg/day significantly prevented development of hyperglycemic as well as hyperinsulinemia.
Consequently, M. charantia might prove useful in the treatment and/or prevention of insulin resistance in non-diabetic state.
1000691 In a study by Shetty et al. in 2005, male Wistar rats were rendered diabetic by a single injection of streptozotocin such that there were two groups of 12 diabetic rats and two groups of 6 age-matched normal rats (control). Bitter gourd (M. charantia) was incorporated at 10% level in the diet and glycemic control of bitter gourd during diabetes was evaluated by monitoring diet intake, gain in body weight, water intake, urine sugar, urine volume, glomerular filtration rate and fasting blood glucose profiles. The administration of bitter gourd showed significant reduction in urine excretion, urine sugar excretion, glomerular filtration rate and fasting blood glucose level. At the end of the experiment, there was approximately 30%
improvement in the fasting blood glucose level and as such it is evident that bitter gourd is beneficial in controlling diabetes status.
[00070] In a study by Shibib et al. (1993), the biochemical mechanism of the hypoglycemic activity of M. charantia was examined in streptozotocin-induced diabetic rats.
The results of this study confirmed the hypoglycemic activity of M. charantia.
This activity was mediated through the suppression of hepatic gluconeogenic enzymes, glucose-6-phosphatase and fructose-1, 6-bisphophatase while stimulating glucose-6-phosphatse dehydrogenase. As such, M.
charantia is consistent with the antihyperglycemic effect reported in literature.
[00071] Most of the experimental studies reported in literature on the antihyperglycemic activity of M. charantia were induced by alloxan or streptozotocin. However, a study by Qakici et al. in 1994 examined the hypoglycemic effect of orally administrated extracts of M. charantia in normoglycemic or cyproheptadine-induced hyperglycemic mice. Streptozotocin or alloxan are known to cause irreversible destruction of insulin-secreting 0-cells in the islets of Langerhans in comparison to cyproheptadine which produces a reversible loss of pancreatic insulin when given in repeated doses. When fed orally, the aqueous extract of M. charantia but not the ethanolic extract showed anti-hyperglycemic and hypoglycemic effects in cyproheptadine-induced hyperglycemic and normoglycemic mice respectively.
1000721 A study undertaken by Sarkar et al. in 1996, demonstrated the hypoglycemic activity of the alcoholic extract of M. charantia in a validated animal model of diabetes mellitus known to respond to oral hypoglycemic drugs. The reduction in plasma glucose level was 10 -15% for M. charantia compared to a decrease of 40 - 44% for tolbutamide, a sulphonylurea drug, under similar conditions. Another finding was that repeated dosing of 500mg/kg of M.
charantia extract did not result in the deterioration of hypoglycemic response in normal rats. In diabetic rats, the oral glucose tolerance was improved causing a significant reduction in plasma glucose of 26% for M. charantia in comparison to metformin which caused a 40 -50%
reduction. The hypoglycemic activity of M. charantia is confirmed in both normal and diabetic animals as reported in the literature with similar responses from oral hypoglycemic drugs such as tolbutamide and metformin.
1000731 In a similar study by Miura et al. (2001), the hypoglycemic activity of the fruit of M. charantia was investigated in an animal model with type 2 diabetes with hyperinsulinemia.
After 3 weeks of oral administration of the water extract of M. charantia, the blood glucose and serum insulin levels were lowered. The results were supportive of the traditional medical use of M. charantia as an antidiabetic agent in type 2 diabetes.
[00074] In a follow up study, the effect of M. charantia with exercise on blood glucose was investigated as the treatment for type 2 diabetes (Miura et al. 2004).
Exercise therapy and diet are usually recommended for type 2 diabetics and as such the inclusion of exercise in this study is investigated. After 5 weeks of oral administration of the water extract of M. charantia fruit with exercise, blood glucose and insulin levels in diabetic rats were significantly reduced. It was lower than that of M. charantia supplementation only or exercise only. The hypoglycemic effect of M. charantia with exercise is a synergistic effect that is beneficial in type 2 diabetics.
[00075] The amount of research reported in literature on the beneficial effects of M.
charantia are mostly concentrated on its antidiabetic activity despite the possibility that it might affect lipid metabolism due to the interconnection between carbohydrate and lipid metabolism (Senanayake et al. 2004 (a)). People with diabetes mellitus are at a higher risk of developing heart disease and other blood vessel diseases as such there have been studies reporting hypertriglyceridaemia and hypercholesterolaemia in diabetic subjects (Chaturvedi 2005). There are a few experimental studies reported in literature that have examined the effect of M.
charantia on triglyceride and cholesterol levels in normal and chemically induced diabetic animals.
1000761 In a study by Jayasooriya et al. in 2000, the effects of dietary freeze-dried powdered bitter melon on serum glucose level and lipid parameters of serum and liver were examined in rats fed with and without cholesterol. Male Sprague-Dawley rats were fed the diets for 14 days at 0.5, 1 and 3% without added dietary cholesterol and at a level of 1% with or without added cholesterol and 0.15% bile acid. Dietary bitter melon consistently decreased serum glucose levels in rats fed cholesterol-free diets. The addition of bitter melon to cholesterol-free and cholesterol-enriched diets caused an elevated serum HDL-cholesterol level, an indication of antiatherogenic activity. Also, there was a consistent reduction of hepatic total cholesterol and triglyceride levels both in the presence and absence of dietary cholesterol where the reduction of triglyceride concentrations, in absence of dietary cholesterol, was in a dose-dependent manner. These results suggest that bitter melon contains components which influence the metabolism of serum and liver lipids such that it may improve and/or ameliorate lipid disorders such as hyperlipidemia and fatty liver.
[00077] In 2001, Ahmed et al. performed a study to investigate the long term effect of MC
fruit extract on blood plasma and tissue lipid profiles in normal and streptozotocin (STZ)--induced type 1 diabetic rats. Male Wistar rats were induced diabetic with a single intraperitoneal injection of a buffered solution of STZ at a dosage of 60 mg/kg body weight.
The animals were divided into four groups of six: diabetic, diabetic treated with karela extract, karela treated control and untreated control group. There was a significant increase in plasma non-esterified cholesterol, triglycerides and phospholipids in the diabetic rats accompanied by a decrease in HDL-cholesterol. However, over a 10-week treatment period with MC fruit extract, these levels returned close to normal. Also, under in vitro conditions, karela juice exhibited an inhibitory effect on membrane lipid peroxidation in a dose-dependant manner due to some antioxidant components present in the fruit extract. This study shows that besides its known hypoglycemic properties, karela fruit extract also exhibits strong hypolipidemic action on diabetic hypertriglyceridemia and hypercholesterolemia. Additionally, it has some antioxidative properties which contribute towards preventing lipid peroxidative damage.
1000781 In a study by Chen et al. (2003), the energy efficiency and adiposity of male rats were investigated with 0.375, 0.75 and 1.5% of bitter melon supplementations in high fat and low fat diets. Rats on the high fat diet with 1.5% bitter melon gained less weight and had less visceral fat than those fed the high fat diet. Bitter melon supplementation did not change apparent fat absorption but improved insulin resistance, lowered serum insulin and leptin but raised serum free fatty acid concentrations. The reduction of adiposity in rats fed a high fat diet indicates bitter melon has influences on lipid metabolism other than glucose metabolism.
1000791 Chen et al. carried out another study in 2005 to further investigate the metabolic consequences and possible mechanism(s) of the above study results. Bitter melon supplementation of 0.75 or 1.5% in either low-fat or high-fat diet had lower energy efficiency, visceral fat mass, plasma glucose and hepatic triacylglycerol but higher serum free fatty acids and plasnia catecholamines indicating an enhanced sympathetic activity and lipolytic process.
This clearly demonstrated the ability of bitter melon supplementation to reverse steatosis and normalize hepatic triacylgleycerol.
[00080] In a study by Senanayake et al. (2004 (b)), the effects of three different varieties of bitter melon on serum and liver lipids were examined. The effects on serum lipid parameters were marginal for all three varieties. On the other hand, all three varieties of bitter melon lowered hepatic triglyceride levels but the Koimidori variety was found to be the most effective.
Further investigation on this variety was carried out on finding the active component(s) of bitter melon responsible for liver triglyceride lowering activity by fractionation the bitter melon using organic solvents such as n-hexane, acetone, and methanol. The liver triglyceride levels in rats fed diets containing the methanol fraction at 1% level was similar to those fed unfractionated Koimidori at 3%. Therefore, the potent active component of bitter melon lowering liver triglyceride concentrations is found to be concentrated in the methanol fraction. The methanol fraction was able to lower liver cholesterol concentration in a dose-dependent manner. Hence, bitter melon is useful in relieving and/or ameliorating life style-related diseases such as fatty liver, hypertriglyceridemia and diabetes.
[00081] The authors from the above study carried out a very similar experiment using only the bitter melon of the Koimidori variety at levels of 0.5 and 1% to examine its hypolipidemic effect in Syrian hamsters fed a diet supplemented with and without 0.2%
cholesterol (Senanayake et al. 2004(a)). The serum triglyceride-lowering activity of dietary methanol fraction extracted from bitter melon was observed in a dose-dependent manner in hamsters fed diets with no added cholesterol. This dose-dependent triglyceride lowering effect was also seen in hamsters fed cholesterol-enriched diet supplemented with bitter melon. Even though elevated liver triglyceride levels were caused by the dietary cholesterol, these levels were still lower with bitter melon supplements. As a result, dietary bitter melon extract is effective in lowering serum and liver triglyceride especially in those with hypertriglyceridemia caused by dietary cholesterol.
1000821 In a more detailed study by Chaturvedi et al. (2004), the methanol extract of the fruit M. charantia was administered to diabetic rats to assess the long term effect of the extract on lipid profile and oral glucose tolerance test. After 30 days treatment, there was a significant reduction in triglyceride and LDL, and a significant increase in HDL level. A
significant effect on oral glucose tolerance was also noted but more obvious when the extract was given on the same day as the test.
1000831 In 2005, Chaturvedi performed a study to assess whether or not a methanol extract of M. charantia was able to normalize lipid and glucose levels in diabetic rats fed a high-fat and low-carbohydrate diet. Different doses of the extract were administered to alloxan-induced diabetic albino rats of the Horts Men strain for 45 days. Blood glucose, triglyceride, LDL and HDL levels showed a dose-dependent response to M. charantia extract while cholesterol levels were found to be significantly lower. M. charantia extract normalized blood glucose level, reduced triglyceride and LDL levels and increased HDL level. Hence, M.
charantia can play an active part in the management of diabetes and have a positive impact on factors responsible for heart diseases and other related disorders.
1000841 To date there have been no formal pharmacokinetic studies done on this plant in animals or humans. This may be due to the fact that they are commonly consumed as a vegetable. Hence, the absorption of bitter melon occurs in the intestinal tract. It is absorbed into the blood to affect glucose metabolism and incorporated into hepatic tissues to influence the metabolism of triglyceride (Jayasooriya et al. 2000 and Senanayake et al. 2004 (b)). The i i pharmacologic effects of the insulin-like polypeptide contained in bitter melon have an onset ction between 30 and 60 minutes and a peak effect at about four hours (Jellin et al. 2005).
[00085] The exact mechanism of action of Momordica charantia in animals and humans has not been elucidated; however investigators have proposed many plausible theories based on experimental results.
[00086] This effect seems to be through a number of different mechanisms. One of the earlier theory was that a component of bitter melon extract, polypeptide-p, have structural similarities to bovine insulin and as such the hypoglycemic activity (Khanna et al. 1981 and Basch et al. 2003). Other hypoglycemic chemicals of Momordica charantia include a mixture of steroidal saponins known as charantin, momordin Ic, oleanolic acid 3-0-monodesmoside and oleanolic acid 3-0-glucuronide (Grover and Yadav 2004). The mechanisms proposed for effects on glucose and insulin include an inhibitory effect on glucose absorption in the intestine by decreasing hepatic gluconeogenesis, increasing hepatic glycogen synthesis and increasing peripheral glucose oxidation (Shibib et al. 1993 and Basch et al. 2003), enhanced insulin release from beta cells (Sitasawad et al. 2000 and Saxena and Vikram 2004) and an extrapancreatic effect via increased glucose uptake by tissues and increased GLUT4 transporter protein of muscles (Day et al. 1990, Sarkar et al. 1996 and Miura et al. 2001).
[00087) The hypolipidemic effect of Momortica charantia has not been as extensively studied as the hypoglycemic effect; however, the mechanism of action that has been proposed by investigators based on experimental studies include controlling the hydrolysis of certain lipoproteins through enhanced sympathetic activity, lipolysis and possibly lipid oxidation, for selective uptake and metabolism by different tissues (Ahmed et al. 2001, Chen et al. 2003 and Chen and Li 2005), and bitter melon contains some active components, saponin and plant sterols that are known to have an inhibitory effect on lipid biosynthesis thus lowering liver triglyceride levels in animals and inhibiting cholesterol absorption in the intestinal tract (Senanayake et al.
2004 (a & b)). The strong antihyperlipidemic effect of M. charantia could also be explained through its control of hyperglycemia as insulin is a major determinant of total and very low density lipoprotein and triglyceride concentration (Ahmed et al. 2001). The hyperlipidemia observed in diabetics is a consequence of uninhibited action of lipolytic hormones on fat depots as insulin inhibits adipose tissue hormone-sensitive lipase reducing lipolysis and mobilization of peripheral depots (Ahmed et al. 2001).
[00088] Much literature has been published on bitter melon and cinnamon. A
partial listing of the published research on bitter melon is provided in Schedule A
and a partial listing of the published research on cinnamon is provided in Schedule B.
[00089] The present inventors have shown that the new therapeutic formulation comprising cinnamon and bitter melon demonstrates synergist activity and inter alia:
(a) healthy glucose level for people with type 2 diabetes;
(b) optimum level of cholesterol and triglycertides for people of all ages and thus reduces the risk of cardiovascular disease.
[00090] Thee new therapeutic formulation has also been proven as a powerful antioxidant and effective in helping to prevent cancer, heart disease, and stroke.
[00091] Another major benefit of the new therapeutic formulation is that it can prevent insulin resistance, a major and common complication that develops in people with type II
diabetes in later years.
[00092] The two main ingredients of the new therapeutic formulation come from cinnamon and bitter melon, two natural products with long history both as foods and as medicines. Both the ingredients have been successfully used as effective remedies for many medical conditions in Indian, Chinese and South American Traditional Medicine.
[00093] The mechanism of actions are different from one another as cinnamon activates the insulin kinase receptor to increase insulin sensitivity through insulin-mimetic activity while the mechanisms for bitter melon include increased insulin secretion, tissue glucose uptake, liver muscle glycogen synthesis, glucose oxidation and decreased hepatic gluconeogenesis. As a result, combining these two ingredients has a synergistic effect which would lead to greater benefits for people with diabetes. Also, it has been observed that people with diabetes are usually associated with hypertriglyceridemia and hypercholesterolemia.
Therefore, the combination of cinnamon and bitter melon has the potential to treat and prevent diabetes and other related cardiovascular diseases by lowering blood glucose levels and normalizing lipid profiles. Therefore, the combination of the medicinal ingredients is both novel and innovative.
[00094] The ratio of cinnamon to bitter melon may be varied and it is preferred that it be between sixty to seventy percent (60 - 70%) of cinnamon and forty to thirty percent (40 - 30%) of bitter melon.
1000951 One new therapeutic formulation contains cinnamon and bitter melon at a ratio of 60:40 which is the most synergistic combination of the two plants for the management of blood sugar levels of type 2 diabetes patients as well as for normalizing the lipid profiles. The new therapeutic formulation also contains the highest concentration of water soluble flavonoids extracted from cinnamon ( the part of the cinnamon extract responsible for its blood sugar lowering effect) compared to any other similar products in the market.
1000961 In order to achieve the desired synergism, the dosage of bitter melon should in the range of 100 to 200 milligrams two to three times a day with at least one gram of cinnamon per day. A particularly useful preparation is a 500 milligram capsule containing about 200 milligrams of bitter melon and 300 milligrams of cinnamon and one capsule should be taken twice a day to achieve the desired dosage.
[00097] Examples:
One particularly useful formulation is as follows:
Cinnamon (Cinnamomi cassiae: Cinnamonum verum) 280 mg Bitter melon (Momordica charantia) 120 mg Diluent 151 mg Lubricant 3 mg [00098] The bark of cinnamon was used in a ratio of 10:1 to produce the active ingredient.
Similarly, the whole melon was used in a ration of 10:1 to produce the desired amount of bitter melon. As the diluent, it was found useful to use microcrystalline cellulose in the amount of 150 milligrams mixed with one (1) milligram of dicalcium phosphate dihydrate.
Magnesium stearate was used as the lubricant. The ingredients were mixed and placed in a gelatin capsule.
Administration was also found to lower blood sugar levels and to normalize lipid profiles.
100991 One of the more difficult challenges for a manufacturer of a product which is orally ingested is to produce that product in a vehicle which encourages use of the product and which is attractive to the consumer. In this regard, the inventors have found that the new herbal product of the present invention may be incorporated into a vehicle which is chocolate based which would make the product much more palatable and attractive to the consumer.
[00100] In this regard, a product formulation has been invented which incorporates the novel herbal product into a vehicle comprised substantially of chocolate.
Although the product may be incorporated into any suitable chocolate vehicle, a particularly useful process and product is hereinafter described.
1001011 It has been found that certain chocolate form better vehicles than others. In particular, it is desired to use a sugar free chocolate formulation to avoid additional sugar in the final product.
[00102] The inventors have found the following four particularly useful formulations for the chocolate vehicle. Each of the following formulations do not contain any added sugar and are commercially available.
1001031 The first formulation is a dark chocolate which comprises forty-three percent (43%) maltitol, cocoa butter and cocoa powder processed with an alkali. A
chocolate liquor and cocoa powder along with milk fat and soya lecithin which is used as the emulsifier, and natural flavours are added.
[00104] A second formulation relates to a milk chocolate which contains maltitol in the amount of fifty-five percent (55%), cocoa butter and a chocolate liquor.
Calcium carbonate and milk fat are added as well as calcium caseinate and soya lecithin as the emulsifier with vanilla extract for taste.
[00105] A third useful formulation is a high protein sucrose free milk chocolate which includes maltitol, fractionated modified palm kernel oil, milk protein concentrate and cocoa powder. Calcium caseinate, soya lecithin as the emulsifier and vanilla extract are used.
[00106] The fourth formulation is a dark sugar free coating which is comprised of a chocolate liquor processed with an alkali, maltitol, cocoa butter, butter oil, soya lecithin as the emulsifier and vanilla extract.
[00107] The inventors have found the following process to be particularly useful.
[001081 The chocolate is first melted to a minimum temperature of ninety-five degrees Fahrenheit (95 F) to a maximum of one hundred and twenty degrees Fahrenheit (120 F).
Preferably, the chocolate is placed within a water jacketed kettle which has an agitator. After melting of the chocolate, the jacket is cooled to a temperature of sixty degrees Fahrenheit (60 F) to a maximum of ninety degrees Fahrenheit (90 F). The chocolate is allowed to cool to a minimum of sixty-eight degrees Fahrenheit (68 F) to a maximum of eight-nine degrees Fahrenheit (89 F) with the agitator running. The agitator continues to run until the chocolate starts to thicken.
[00109] After the chocolate has thickened, the jacket is gradually warmed to a temperature of a minimum of eighty degrees Fahrenheit (80 F) with the agitator running.
The chocolate is warmed to a temperature between eight-five degrees Fahrenheit (85 F) to ninety-five degrees Fahrenheit (95 F) with the agitator running and the herbal product is then added to this warmed chocolate in slow measures with the agitator running. The product is thoroughly mixed and when the mixing is completed, the jacket temperature is reduced. The chocolate is then poured into molds and cooled in a cooling tunnel.
1001101 It is preferred that the molds in which the chocolate is poured are kept at a temperature between seventy-eight degrees Fahrenheit (78 F) and eighty-two degrees Fahrenheit (82 F). The cooling tunnel subjects the chocolate in the mold to an initial cooling at a temperature between sixty-five degrees Fahrenheit (65 F) and seventy degrees Fahrenheit (70 F), to a main cooling stage between forty-five degrees Fahrenheit (45 F) to fifty degrees Fahrenheit (50 F) and to a final cooling stage of between sixty-five degrees Fahrenheit (65 F) to seventy degrees Fahrenheit (70 F).
[001111 It is preferred that for every forty (40) grams of chocolate, the product will contain between one hundred and fifty (150) milligrams to a maximum of one thousand (1000) milligrams of the cinnamon and to between one hundred (100) milligrams to one thousand (1000) milligrams of the bitter melon.
[00112] This produces an excellent product which finds wide acceptance with the consumer in view of the chocolate vehicle.
[00113] The inventors have also found that a more improved product can be produced when omega-3 fatty acids are added to the chocolate mix, preferably as a powder.
[001141 Omega-3 fatty acids are polyunsaturated fatty acids classified as essential because they cannot be synthesised in the body. Accordingly, they must be obtained from food. A good source of omega-3 fatty acids is fish oil. Essential fatty acids are essential to normal growth in young children and animals. A small amount of omega-3 fatty acids in the diet enables normal growth. It has now been found that there is a demonstrable link between omega-3 fatty acids and cancer protection. Further, it is known that omega-3 fatty acids significantly reduce blood triglyceride levels. Elevate triglyceride levels are associated with increased risk for cardiovascular disease, especially in women. Accordingly, it has been found that omega-3 fatty acids when introduced into the diet, will reduce high blood pressure and have an anti-inflammatory property.
1001151 Support can be found in the literature. For example, the following reference demonstrate the improved health effects of omega-3 fatty acids when introduced into the diet.
Suitable references include:
Robinson JG, Stone NJ. Antiatherosclerotic and antithrombotic effects of omega-3 fatty acids. Am J Cardiol. 2006 Aug 21;98(4A):39i-49i. Epub 2006 May 30. Review.
Psota TL, Gebauer SK, Kris-Etherton P. Dietary omega-3 fatty acid intake and cardiovascular risk. Am J Cardiol. 2006 Aug 21;98(4A):3i-18i. Epub 2006 May 30.
Review.
Hooper L, Thompson RL, Harrison RA, Summerbell CD, Ness AR, Moore HJ, Worthington HV, Durrington PN, Higgins JP, Capps NE, Riemersma RA, Ebrahim SB, Davey Smith G. Risks and benefits of omega-3 fats for mortality, cardiovascular disease, and cancer: systematic review. BMJ. 2006 Apr 1;332(7544):752-60. Epub 2006 Mar 24.
Review.
Shahidi F, Miraliakbari H. Omega-3 fatty acids in health and disease: part 2--health effects of omega-3 fatty acids in autoimmune diseases, mental health, and gene expression. J Med Food. 2005 Summer;8(2):133-48. Review 1001161 The human body can produce all but two of the fatty acids it needs.
The two fatty acids that the body cannot produce are widely distributed in fish oils. Since they cannot be made in the body from other substrates and must be supplied in food, they are called essential fatty acids. In the body, essential fatty acids are primarily used to produce hormone-like substances that regulate a wide range of functions, including blood pressure, blood clotting, blood lipid levels, the immune response and the inflammation response to injury infection.
1001171 Essential fatty acids are polyunsaturated fatty acids and are apparent compounds of, inter alia, omega-3 fatty acids. They are important in several human body systems including the immune system and in blood pressure regulation. They are used to make compounds such as prostaglandis the two most important long chain polyunsaturated fatty acids are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
[00118] Eicosapentaenoic acid (EPA) is an omega-3 essential fatty acid that acts as a precursor for prostaglandin-3 which inhibits patelet aggregation. It is commony found in fish oils from cod liver, herring, mackerel, salmon and sardine and it is also found in human breast milk. A large number of conditions in which EPA acts alone or with other omega-3 sources is thought to be effective including lowering inflammation.
[00119] Docosahexaenoic acid (DHA) is a major fatty acid in sperm and brain phospholipids, especially in the retina. Dietary DHA can reduce the level of blood triglycerides in humans, which may reduce the risk of heart disease. Low levels of DHA have been associated with Alzheimer's disease, depression and other diseases and there is evidence that DHA
supplementation may be effective in combating such diseases.
[00120] The omega-3 fatty acids is preferably supplied as a powder although there are forms which are available.
[00121] The novel product is made exactly as is the chocolate product using the same recipe except after the chocolate is fully added and mixed, then the omega-3 is added, preferably as a powder, immediately before the reduction of the jacket temperature. The amount of omega-3 added can vary between a minimum of 100 mg to a maximum of 1000 mg per 40 gm of final product.
[00122] Although the disclosure describes a preferred embodiment, the invention is not so limited. For a definition of the invention, reference is made to the claims.
SCHEDULE A
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U.S. Patents:
PAT. NO. Title 1 7,014,872 Herbal nutraceutical formulation for diabetics and process for preparing the same 2 6,964,786 Oil from Momordica charantia L., its method of preparation and uses 3 6,960,348 Goya derived cosmetic compositions for face and bodX
4 6,831,162 Protein/polypeptide-k obtained from Momordica charantia and a process for the extraction thereof 6,800,726 Proteins with increased levels of essential amino acids 6 6,770,585 Momordica cochinchinensis (Spreng.) .beta.-carotene and method 7 6,562,379 Adult-onset diabetes treatment method 8 6,379,718 Use of plant extracts for treatment of acne and furuncle 9 6,235,286 Adult-onset diabetes treatment method 6,183,747 Use of plant Momordica charactia extracts for treatment of acne acid 11 6,103,240 Herbal sweetening and preservative composition comprising licorice extract and mogrosides obtained from plants belonging to cucurbitaceae and/or momordica 12 5,942,233 Herbal composition for stimulating blood circulation 13 5,929,047 Anti-viral agent prepared by basic and acidic extraction of mangraves 14 5,900,240 Herbal compositions and their use as hypoglycemic agents 5,851,531 Adult-onset diabetes treatment method 16 5,484,889 Plant protein useful for treating tumors and HIV infection 17 4,368,149 Protein hybrid having c otoxicity and process for the preparation thereof 18 4,084,010 Glycosides having sweetness 1: Khan B, Arayne MS, Naz S, Mukhtar N.
Hypogylcemic activity of aqueous extract of some indigenous plants.
Pak J Pharm Sci. 2005 Jan;18(1):62-4.
PMID: 16431387 [PubMed - indexed for MEDLINE]
2: Reyes BA, Bautista ND, Tanquilut NC, Anunciado RV, Leung AB, Sanchez GC, Ma tg oto RL, Castronuevo P, Tsukamura H, Maeda KI.
Anti-diabetic potentials of Momordica charantia and Andrographis paniculata and their effects on estrous cyclicity of alloxan-induced diabetic rats.
J Ethnopharmacol. 2005 Nov 16; [Epub ahead of print]
PMID: 16298503 [PubMed - as supplied by publisher]
3: Ansari NM, Houlihan L, Hussain B, Pieroni A.
Antioxidant activity of five vegetables traditionally consumed by South-Asian migrants in Bradford, Yorkshire, UK.
Phytother Res. 2005 Oct;19(10):907-11.
PMID: 16261524 [PubMed - indexed for MEDLINE]
4: Yang X, Kong C, Liang W, Zhang M, Hu F.
[Relationships of Aulacophora beetles feeding behavior with cucurbitacin types in host crops]
Ying Yong Sheng Tai Xue Bao. 2005 Jul;16(7):1326-9. Chinese.
PMID: 16252877 [PubMed - in process]
5: Dengiz GO, Gursan N.
Effects of Momordica charantia L. (Cucurbitaceae) on indomethacin-induced ulcer model in rats.
Turk J Gastroenterol. 2005 Jun;16(2):85-88.
PMID: 16252198 [PubMed - as supplied by publisher]
6: Chan LL, Chen Q, Go AG, Lam EK, Li ET.
Reduced adiposity in bitter melon (Momordica charantia)-fed rats is associated with increased lipid oxidative enzyme activities and uncoupling protein expression.
J Nutr. 2005 Nov;135(11):2517-23.
PMID: 16251604 [PubMed - indexed for MEDLINE]
7: Shekelle PG, Hardy M, Morton SC, Coulter I, Venuturupalli S, Favreau J, Hilton LK.
Are Ayurvedic herbs for diabetes effective?
J Fam Pract. 2005 Oct;54(10):876-86. Review.
PMID: 16202376 [PubMed - indexed for MEDLINE]
8: Chaturvedi P.
Role of Momordica charantia in maintaining the normal levels of lipids and glucose in diabetic rats fed a high-fat and low-carbohydrate diet.
Br J Biomed Sci. 2005;62(3):124-6.
PMID: 16196458 [PubMed - indexed for MEDLINE]
9: Mekuria DB, Kashiwagi T, Tebayashi S, Kim CS.
Cucurbitane triterpenoid oviposition deterrent from Momordica charantia to the leafrniner, Liriomyza trifolii.
Biosci Biotechnol Biochem. 2005 Sep;69(9):1706-10.
PMID: 16195588 [PubMed - indexed for MEDLINE]
10: Girini MM, Ahamed RN, Aladakatti RH.
Effect of graded doses of Momordica charantia seed extract on rat sperm:
scanning electron microscope study.
J Basic Clin Physiol Pharmacol. 2005;16(1):53-66.
PMID: 16187486 [PubMed - indexed for MEDLINE]
11: Shetty AK, Kumar GS, Sambaiah K, Salimath PV.
Effect of bitter gourd (Momordica charantia) on glycaemic status in streptozotocin induced diabetic rats.
Plant Foods Hum Nutr. 2005 Sep;60(3):109-12.
PMID: 16187012 [PubMed - indexed for MEDLINE]
12: Hsieh CL, Lin YC, Ko WS, Peng CH, Huang CN, Peng RY.
Inhibitory effect of some selected nutraceutic herbs on LDL glycation induced by glucose and glyoxal.
J Ethnopharmacol. 2005 Dec 1;102(3):357-63. Epub 2005 Sep 12.
PMID: 16162395 [PubMed - indexed for MEDLINE]
13: Long-Yun L, Shu S, Wei YF, Zhong GY, Chen JH.
[Morphological and histological studies of Herpetospermum pedunculosum seeds and other substitutes]
Zhongguo Zhong Yao Za Zhi. 2005 Jul;30(14):1073-6. Chinese.
PMID: 16161440 [PubMed - in process]
14: Li LY, Deji LM, Wei YF, Zhong GY.
[Literature data investigation in semem of Herpetospermum pedunculosum]
Zhongguo Zhong Yao Za Zhi. 2005 Jun;30(12):893-5. Chinese.
PMID: 16124602 [PubMed - in process]
15: Zheng ZX, Teng JY, Liu JY, Qiu JH, Ouyang H, Xue C.
[The hypoglycemic effects of crude polysaccharides extract from Momordica charantia in mice]
Wei Sheng Yan Jiu. 2005 May;34(3):361-3. Chinese.
PMID: 16111053 [PubMed - in process]
16: Mutalik S, Chetana M, Sulochana B, Devi PU, Udupa N.
Effect of Dianex, a herbal formulation on experimentally induced diabetes mellitus.
Phytother Res. 2005 May;19(5):409-15.
PMID: 16106394 [PubMed - indexed for MEDLINE]
17: Akhtar S, Ali Khan A, Husain Q.
Partially purified bitter gourd (Momordica charantia) peroxidase catalyzed decolorization of textile and other industrially important dyes.
Bioresour Technol. 2005 Nov;96(16):1804-11. Epub 2005 Feb 25.
PMID: 16051087 [PubMed - indexed for MEDLINE]
18: Raj SK, Khan MS, Singh R, Kumari N, Prakash D.
Occurrence of yellow mosaic geminiviral disease on bitter gourd (Momordica charantia) and its impact on phytochemical contents.
Int J Food Sci Nutr. 2005 May;56(3):185-92.
PMID: 16009633 [PubMed - indexed for MEDLINE]
19: Kumar Shetty A, Suresh Kumar G, Veerayya Salimath P.
Bitter gourd (Momordica charantia) modulates activities of intestinal and renal disaccharidases in streptozotocin-induced diabetic rats.
Mol Nutr Food Res. 2005 Aug;49(8):791-6.
PMID: 16007724 [PubMed - indexed for MEDLINE]
Cinnamon bark has been used medicinally in China since 2700 B.C.E and is said to supplement vital energy and blood, tone the kidney and spleen and acts as an antioxidant (Blumenthal et al.
1998). Cinnaniomum aromaticum has also been used in Korea, China and Russia as a traditional folk herb with hypoglycemic properties for the treatment of diabetes mellitus (Kim et al. 2005).
The increasing prevalence of diabetes and cardiovascular disease is evident worldwide with an estimated 1700 new cases diagnosed daily (Jarvill-Taylor et al. 2001).
Additionally, several million people worldwide are suffering from 'pre-diabetes' caused by high glucose levels with a resistance to insulin (Khan et al. 2003). The primary function of insulin is to maintain low blood glucose, lipid and cholesterol levels to maintain a sense of well-being.
Environmental factors such as diet, exercise, and stress also attribute to decreasing insulin sensitivity and increasing glucose and low-density lipoprotein (LDL) cholesterol levels, increasing the risk of cardiovascular diseases, obesity, dyslipidemias, diabetes mellitus and premature aging. The increase in disease is partly due to the augmented intake of calories and refined carbohydrates, lesser consumption of fibers and a more sedentary lifestyle. Controlling dietary intake and exercise could prevent disease but the majority of individuals require an extra aid to maintain normal health (Talpur et al., 2005). There is a growing interest in herbal remedies due to the side effects associated with therapeutic hypoglycemic agents and insulin (Kim et al. 2005).
Botanical products with a long history of safety are widely used to lower glucose, lipid and cholesterol levels and for the prevention and treatment of diabetes.
[000171 Cinnamomum aromaticum has been used as a hypoglycemic agent in ancient medicines (Kim et al. 2005). The modem therapeutic properties of cinnamon are supportable based on thousands of years of use in well established systems of traditional medicines, as well as some modem clinical studies (Blumenthal et al. 1998). A number of well proven in vivo animal studies on Cinnamomum aromaticum demonstrate that activation of the insulin receptor increases autophosphorylation resulting in an increase in glucose uptake and glycogen synthesis.
However, there is a limited amount of published data on the effects of cinnamon consumption on blood glucose in humans. In vivo, in vitro and human studies have established that cinnamon extract regulates insulin activity and reduces serum glucose and cholesterol levels (Khan et al.
2003 and Kim et al. 2005).
[00018] In a study by Khan et al. in 2003, 60 men and women with type 2 diabetes ingested daily doses of cinnamon or placebo capsules for 40 days followed by a 20-day washout period. Cinnamon capsules contained 1, 3 or 6 g of Cinnamomum aromaticum.
After 20 days, only the 6 g cinnamon group showed significantly lower glucose levels.
However, after 40 days, serum glucose (18-29%), triglycerides (23-30%) and total cholesterol (12-26%) concentrations were significantly lower in all cinnamon groups. Total cholesterol was lower in all groups at 40 days but low-density lipoprotein (LDL) concentrations were only significantly lower in the 3 g and 6 g cinnamon groups (10% and 24%, respectively). For the 1 g cinnamon group, LDL
concentrations continued to decline during the washout period and were significant at 60 days (P<0.05). The decreased concentration of glucose was maintained by the 1 g cinnamon group while triglyceride and total cholesterol levels were maintained in all cinnamon groups throughout the 20-day washout period.
[00019] Vanschoonbeek et al. 2006 performed a 6 week standardized placebo-controlled study to investigate the proposed benefits of Cinnamomum cassia on 25 postmenopausal women diagnosed with type 2 diabetes. Patients were divided into two groups and supplemented with 1.5 g/day of Cinnamomum or placebo to assess the effects on glucose tolerance and whole-body insulin sensitivity. At 0, 2 and 6 weeks oral glucose tolerance tests and blood lipid profiles were performed resulting in no time x treatment interaction observed for fasting glucose, insulin concentration, insulin resistance, (oral glucose) insulin sensitivity or fasting blood lipid concentrations. This study shows cinnamon supplementation does not have a health benefit in patients with type 2 diabetes contradicting the results found by Khan et al.
2003. Differences between the two studies could be attributed to the selection of patients and the combination of medications taken. In the current study, only postmenopausal female patients were included and continued using commonly prescribed combinations of oral blood glucose-lowering agents, which was not a factor in the study by Khan et al. 2003, explaining the low baseline values found in the patients used in the current study. Although the authors concluded cinnamon supplementation in combination with oral blood glucose-lowering agents may not be beneficial to overweight, postmenopausal women, this is a small concentrated study not factoring in the use of other medications and patient characteristics.
[000201 In a study by Talpur et al. in 2005, Zucker fatty rats (ZFRs) and spontaneously hyper-tensive rats (SHRs) were fed water or essential oils in acute or chronic doses to assess the effect of essential oil combinations on insulin sensitivity. The essential oil treatment consisted of 8 essential oils including cinnamon. Insulin sensitivity was determined by systolic blood pressure (SBP) and a glucose tolerance test. In the acute study, ZFRs and SHRs with essential oil treatments showed significant decreases in SBP at 4, 10 and 20 hours and at 4 hours, respectively. However, SBP levels were equal to the control group at 30 hours in ZFRs and at 10, 20 and 30 hours in SHRs. In the chronic study, ZFRs and SHRs consuming the essential oils showed significantly lower SBP at 8, 17 and 25 days in comparison to the control group.
Decreases in SBP levels ranged from 11 to 20 mmHg. During the oral glucose test, ZFRs consuming the essential oil combination showed consistently lower levels of circulating insulin, however these results were not significant. SHRs did not produce any effect on insulin levels and were equal to the controls, paralleling previous studies where effects were only produced when rats were challenged in stress-free environments (Verspohl et al. 2005).
The decreases in SBP and circulating glucose levels, produced by both species of rats, enhance insulin sensitivity and parallels the idea that fluctuating SBP is the most sensitive index of insulin sensitivity.
Cinnamon has been shown to have insulin-like actions and affect insulin signaling (Broadhurst et al. 2000), and as an ingredient in the essential oil combination it may have a role in the reduction of SBP.
[00021] In another study, Kim et al. 2006, administered db/db mice Cinnamomum cassia dosages of 50, 1.00, 150 or 200 mg/kg for 6 weeks to determine its effect on blood glucose. The control group showed high blood glucose levels at 2, 4, and 6 weeks. The cinnamon extract-treated group showed significantly lower blood glucose levels at each time period (P<0.05, <0.01 and <0.001). Significant decreases in triglyceride and total cholesterol levels were noted in the cinnamon extract group. Similar to Khan et al. 2003 these results parallel the hypoglycemic effects in the cinnamon extract-treated group as reduced levels are maintained for a long period of time.
1000221 In a similar study by Verspohl et al. in 2005, blood glucose and plasma insulin levels were evaluated in Wistar rats given extracts of Cinnamomum bark, cassia or zeylanicum.
During the glucose tolerance test, plasma insulin levels increased significantly after the administration of Cinnamomum extracts with cassia showing the most pronounced effect. The saline placebo group showed no effect on plasma insulin. In all extract-treated groups, blood glucose levels did not decrease unless the rat was challenged by a glucose tolerance test in a stress-free environment. Cinnamomum cassia produced a direct insulin stimulatory effect showing superior effects compared to zeylanicum.
[00023] The increase in fructose consumption has risen worldwide in the past two decades as a significant proportion of energy intake in the diet. Qin et al. 2004 fed 18 male Wistar rats a high-fructose diet and 6 a control diet for 3 weeks to determine the effects of glucose utilization and insulin sensitivity. 12 of the rats consuming a high-fructose diet had Cinnamomum cassia extracts (300 mg/kg/day) added to their diet. During the euglycemic clamp procedure to measure glucose infusion rates (GIR), the 6 rats consuming only a high-fructose diet showed significant decreases (p<0.0001) in glucose infusion rates while cinnamon treated rats produced significant increases, similar to the controls. The consumption of a high-fructose diet, an environmental factor contributing to diabetes, is common in the western society; the addition of Cinnamomum cassia extract to the diet shows a preventative effect, through an increase in glucose utilization and insulin sensitivity.
[000241 In another study, the effect of cinnamon extract on insulin action was evaluated in Wister rats. Qin et al. 2003 randomly assigned 18 rats into three groups:
saline, 30mg/kg and 300mg/kg cinnamon extract. Cinnamon treatment for 3 weeks did not have an effect on plasma free fatty acids and fasting blood glucose concentrations. Although these levels were not affected in the cinnamon treated group, a difference was prevalent in glucose uptake compared to the placebo group. A dose-dependent manner was noticed with glucose utilization as 300mg/kg enhanced glucose utilization to a greater degree than the 30mg/kg or control groups.
[00025] Methylhydroxychalcone polymer (MHCP), a bioactive compound of cinnamon extract, is hypothesized to trigger an insulin-like response. In a study by Jarvill-Taylor et al.
2001, 3T3-L1 adipocytes were assessed with MHCP to determine its function as an insulin mimetic. Within the first 10 minutes of incubation, the insulin treated adipocytes showed a 2.5 fold increase in glucose transport while the MHCP treated group did not show any increase.
However, gradually over the one-hour period, glucose uptake increased in the MHCP treated group and at 60 minutes, a significant increase was noted. As noted in other studies, the effect of cinnamon did not diminish immediately after stopping treatment. As MHCP is administered, the kinase receptor is activated resulting in phosphorylation of the insulin receptor, a similar effect is seen throughout the insulin signaling pathway.
[00026] A similar study by Broadhurst et al. in 2000 reported an increase in insulin action demonstrated by cinnamon extract in vitro. Rat epididymal adipocytes were given either insulin or cinnamon extract after incubation to determine glucose metabolism. At all dilutions (1:2, 1:10, 1:50) cells exposed to cinnamon extract showed a significant increase in insulin-dependent activity and the effect was maintained at the high dilution (1:50). As adipocytes were treated with cinnamon extract the insulin receptor kinase became activated, a necessary requirement to increase insulin sensitivity. The activation of kinase mimics insulin activity in adipocytes.
Afterwards, active cinnamon extract was incubated with soluble polyvinylpyrrolidone (PVP) to determine if activity was associated with tannins or polyphenols. Cinnamon readily bound to PVP giving it a polyphenolic characterization. With an increase in glucose metabolism, 98% of activity is attributed to PVP indicating the use of phenolics to destroy free radicals that inhibit the activation of insulin-receptor kinase. Cinnamon extract mimics the same mechanism as insulin in adipocytes, increasing insulin sensitivity and glucose metabolism.
[000271 Cinnamomum aromaticum (cinnamon) has convincingly been shown to prevent and control elevated glucose and blood lipid concentrations in both in vitro and in vivo studies and can be maintained for a long period after use. The insulin kinase receptor is activated with cinnamon extract demonstrating insulin-mimetic activity. Elevated glucose and blood lipid concentrations increase the incidence of diabetes and/or cardiovascular health. The use of cinnamon extract can prevent these diseases by regulating the insulin receptor to increase glucose uptake and metabolism.
[00028] To date there have been no formal pharmacokinetic studies done on this plant in animals or humans. The only information derived from literature was a study conducted by Khan et al. in 2003 that found Cinnamomum aromaticum (extract) has a prolonged effect on the human body for 20 days during the washout period. Several animal studies have also shown prolonged effects after consumption of cinnamon extract.
[00029] The exact mechanism of action of Cinnamomum aromaticum (extract) is thought to be that it acts as an insulin-mimetic by activating the kinase receptor and increasing insulin sensitivity. The interaction within the intracellular kinase domain triggers an insulin-like response and stimulates glucose oxidation. Cinnamon also regulates enzymes inside the insulin receptor kinase domain and inhibits both phosphotyrosine-specific protein phosphatase (PTP-1) in vitro and glycogen synthase kinase-3(3 (GSK-3(3) in vivo. The inhibition of PTP-1 keeps the insulin receptor in an activated state and inhibition of GSK-30 stimulates glycogen production.
Cinnamon acts independently from insulin but similar levels of activity were observed proposing that it may activate the same cascade as the insulin signaling pathways (Jarvill-Taylor et al.
2001).
1000301 Cinnamon significantly helps people with type 2 diabetes improve their ability to respond to insulin, thus normalizing their blood sugar levels. Both test tube and animal studies have shown that compounds in cinnamon not only stimulate insulin receptors, but also inhibit an enzyme that inactivates them, thus significantly increasing cells' ability to use glucose. Studies to confirm cinnamon's beneficial actions in humans are currently underway with the most recent report coming from researchers from the US Agricultural Research Service, who have shown that less than half a teaspoon per day of cinnamon reduces blood sugar levels in persons with type 2 diabetes. Their study included 60 Pakistani volunteers with type 2 diabetes who were not taking insulin. Subjects were divided into six groups. For 40 days, groups 1, 2 and 3 were given 1, 3, or 6 grams per day of cinnamon while groups 4, 5 and 6 received placebo capsules. Even the lowest amount of cinnamon, 1 gram per day (approximately '/4 to %2 teaspoon), produced an approximately 20% drop in blood sugar; cholesterol and triglycerides were lowered as well.
When daily cinnamon was stopped, blood sugar levels began to increase.
1000311 Test tube, animal and human studies have all recently investigated cinnamon's ability to improve insulin activity, and thus our cells' ability to absorb and use glucose from the blood.
[00032] Ongoing in vitro or test tube research conducted by Richard Anderson and his colleagues at the USDA Human Nutrition Research Center is providing new understanding of the mechanisnls through which cinnamon enhances insulin activity. In their latest paper, published in the Journal ofAgricultural and Food Chemistry, Anderson et al.
characterize the insulin-enhancing complexes in cinnamon-a collection of catechin/epicatechin oligomers that increase the body's insulin-dependent ability to use glucose roughly 20-fold..
Some scientists had been concerned about potentially toxic effects of regularly consuming cinnamon. This new research shows that the potentially toxic compounds in cinnamon bark are found primarily in the lipid (fat) soluble fractions and are present only at very low levels in water soluble cinnamon extracts, which are the ones with the insulin-enhancing compounds.
[00033] A recent animal study demonstrating cinnamon's beneficial effects on insulin activity appeared in the December 2003 issue of Diabetes Research and Clinical Practice. In this study, when rats were given a daily dose of cinnamon (300 mg per kilogram of body weight) for a 3 week period, their skeletal muscle was able to absorb 17% more blood sugar per minute compared to that of control rats, which had not received cinnamon, an increase researchers attributed to cinnamon's enhancement of the muscle cells' insulin-signaling pathway. In humans with type 2 diabetes, consuming as little as 1 gram of cinnamon per day was found to reduce blood sugar, triglycerides, LDL (bad) cholesterol, and total cholesterol, in a study published in the December 2003 issue of Diabetes Care. The placebo-controlled study evaluated 60 people with type 2 diabetes (30 men and 30 women ranging in age from 44 to 58 years) who were divided into 6 groups. Groups 1, 2, and 3 were given 1, 3, or 6 grams of cinnamon daily, while groups 4, 5, and 6 received 1, 3 or 6 grams of placebo. After 40 days, all three levels of cinnamon reduced blood sugar levels by 18-29%, triglycerides 23-30%, LDL
cholesterol 7-27%, and total cholesterol 12-26%, while no significant changes were seen in those groups receiving placebo. The researchers' conclusion: including cinnamon in the diet of people with type 2 diabetes will reduce risk factors associated with diabetes and cardiovascular diseases.(January 28, 2004) 1000341 The latest research on cinnamon shows that by enhancing insulin signaling, cinnamon can prevent insulin resistance even in animals fed a high-fructose diet! A study published in the February 2004 issue of Hormone Metabolism Research showed that when rats fed a high-fructose diet were also given cinnamon extract, their ability to respond to and utilize glucose (blood sugar) was improved so much that it was the same as that of rats on a normal (control) diet. Cinnamon is so powerful an antioxidant that, when compared to six other antioxidant spices (anise, ginger, licorice, mint, nutmeg and vanilla) and the chemical food preservatives (BHA (butylated hydroxyanisole), BHT (butylated hydroxytoluene), and propyl gallate), cinnamon prevented oxidation more effectively than all the other spices (except mint) and the chemical antioxidants. (May 6, 2004).
[00035] In addition to its unique essential oils, cinnamon is an excellent source of the trace mineral manganese and a very good source of dietary fiber, iron and calcium.
The combination of calcium and fiber in cinnamon is important and can be helpful for the prevention of several different conditions. Both calcium and fiber can bind to bile salts and help remove them from the body. By removing bile, fiber helps to prevent the damage that certain bile salts can cause to colon cells, thereby reducing the risk of colon cancer. In addition, when bile is removed by fiber, the body must break down cholesterol in order to make new bile. This process can help to lower high cholesterol levels, which can be helpful in preventing atherosclerosis and heart disease.
[00036] Cinnamaldehyde (also called cinnamic aldehyde) has been well-researched for its effects on blood platelets. Platelets are constituents of blood that are meant to clump together under emergency circumstances (like physical injury) as a way to stop bleeding, but under normal circumstances, they can make blood flow inadequate if they clump together too much.
The cinnaldehyde in cinnamon helps prevent unwanted clumping of blood platelets. (The way it accomplishes this health-protective act is by inhibiting the release of an inflammatory fatty acid called arachidonic acid from platelet membranes and reducing the formation of an inflammatory messaging molecule called thromboxane A2.) Cinnamon's ability to lower the release of arachidonic acid from cell membranes also puts it in the category of an "anti-inflammatory" food that can be helpful in lessening inflammation.
[00037] Cinnamon's essential oils also qualify it as an "anti-microbial" food, and cinnamon has been studied for its ability to help stop the growth of bacteria as well as fungi, including the commonly problematic yeast Candida. In laboratory tests, growth of yeasts that were resistant to the commonly used anti-fungal medication fluconazole was often (though not always) stopped by cinnamon extracts.
[00038] Cinnamon's antimicrobial properties are so effective that recent research demonstrates this spice can be used as an alternative to traditional food preservatives. In a study, published in the August 2003 issue of the International Journal of Food Microbiology, the addition of just a few drops of cinnamon essential oil to 100 ml (approximately 3 ounces) of carrot broth, which was then refrigerated, inhibited the growth of the food borne pathogenic Bacillus cereus for at least 60 days. When the broth was refrigerated without the addition of cinnamon oil, the pathogenic B. cereus flourished despite the cold temperature. In addition, researchers noted that the addition of cinnamon not only acted as an effective preservative but improved the flavor of the broth.(October 1, 2003) [00039] In addition to the active components in its essential oils and its nutrient composition, cinnamon has also been valued in energy-based medical systems, such as Traditional Chinese Medicine, for its warming qualities. In these traditions, cinnamon has been used to provide relief when faced with the onset of a cold or flu, especially when mixed in a tea with some fresh ginger.
1000401 Bitter melon is of the family Cucurbitaceae, genus Momordica and species charantia. Some synonyms include Momordica chinensis, M. elegans, M. indica, M. operculata, M. sinensis, Sicyosfauriei, and its common names are bitter melon, papailla, melao de sao caetano, bittergourd, balsam apple, balsam pear, karela, k'u kua kurela, kor-kuey, ku gua, pava-aki, salsamino, sorci, sorossi, sorossie, sorossies, pare, peria laut, peria.
It may be used as a whole plant, fruit or seed.
[00041] Bitter melon grows in tropical areas, including parts of the Amazon, east Africa, Asia, and the Caribbean, and is cultivated throughout South America as a food and medicine. It's a slender, climbing annual vine with long-stalked leaves and yellow, solitary male and feniale flowers borne in the leaf axils. The fruit looks like a warty gourd, usually oblong and resembling a small cucumber. The young fruit is emerald green, turning to orange-yellow when ripe. At maturity, the fruit splits into three irregular valves that curl backwards and release numerous reddish-brown or white seeds encased in scarlet arils. The Latin name Momordica means "to bite," referring to the jagged edges of the leaves, which appear as if they have been bitten. All parts of the plant, including the fruit, taste very bitter.
1000421 In the Amazon, local people and indigenous tribes grow bitter melon in their gardens for food and medicine. They add the fruit and/or leaves to beans and soup for a bitter or sour flavor; parboiling it first with a dash of salt may remove some of the bitter taste.
Medicinally, the plant has a long history of use by the indigenous peoples of the Amazon. A leaf tea is used for diabetes, to expel intestinal gas, to promote menstruation, and as an antiviral for measles, hepatitis, and feverish conditions. It is used topically for sores, wounds, and infections and internally and externally for worms and parasites.
1000431 In Brazilian herbal medicine, bitter melon is used for tumors, wounds, rheumatism, malaria, vaginal discharge, inflammation, menstrual problems, diabetes, colic, fevers, worms. It is also used to induce abortions and as an aphrodisiac. It is prepared into a topical remedy for the skin to treat vaginitis, hemorrhoids, scabies, itchy rashes, eczema, leprosy and other skin problems. In Mexico, the entire plant is used for diabetes and dysentery; the root is a reputed aphrodisiac. In Peruvian herbal medicine, the leaf or aerial parts of the plant are used to treat measles, malaria, and all types of inflammation. In Nicaragua, the leaf is commonly used for stomach pain, diabetes, fevers, colds, coughs, headaches, malaria, skin complaints, menstrual disorders, aches and pains, hypertension, infections, and as an aid in childbirth.
[00044] Bitter melon contains an array of biologically active plant chemicals including triterpenes, proteins, and steroids. One chemical has clinically demonstrated the ability to inhibit the enzyme guanylate cyclase that is thought to be linked to the cause of psoriasis and also necessary for the growth of leukemia and cancer cells. In addition, a protein found in bitter melon, momordin, has clinically demonstrated anticancerous activity against Hodgkin's lymphoma in animals. Other proteins in the plant, alpha- and beta-momorcharin and cucurbitacin B, have been tested for possible anticancerous effects. A chemical analog of these bitter melon proteins has been developed and named "MAP-30"; its developers reported that it was able to inhibit prostate tumor growth. Two of these proteins-alpha- and beta-momorcharin-have also been reported to inhibit HIV virus in test tube studies. In one study, HIV-infected cells treated with alpha- and beta-momorcharin showed a nearly complete loss of viral antigen while healthy cells were largely unaffected. MAP-30 has been claimed to be "useful for treating tumors and HIV infections..." Another clinical study showed that MAP-30's antiviral activity was also relative to the herpes virus in vitro.
[00045] In numerous studies, at least three different groups of constituents found in all parts of bitter nielon have clinically demonstrated hypoglycemic (blood sugar lowering) properties or other actions of potential benefit against diabetes mellitus.
These chemicals that lower blood sugar include a mixture of steroidal saponins known as charantins, insulin-like peptides, and alkaloids. The hypoglycemic effect is more pronounced in the fruit of bitter melon where these chemicals are found in greater abundance.
1000461 Alkaloids, charantin, charine, cryptoxanthin, cucurbit, cucurbitaceous, cucurbitanes, cycloartenols, diosgenin, elaeostearic acids, erythrodiol, galacturonic acids, gentisic acid, goyaglycosides, goyasaponins, guanylate cyclase inhibitors, gypsogenin, hydroxytryptamines, karounidiols, lanosterol, lauric acid, linoleic acid, linolenic acid, momorcharasides, momorcharins, momordenol, momordicilin, momordicins, momordicinin, momordicosides, momordin, multiflorenol, myristic acid, nerolidol, oleanolic acid, oleic acid, oxalic acid, pentadecans, peptides, petroselinic acid, polypeptides, proteins, ribosome-inactivating proteins, rosmarinic acid, rubixanthin, spinasterol, steroidal glycosides, stigmasta-diols, stigmasterol, taraxerol, trehalose, trypsin inhibitors, uracil, vacine, v-insulin, verbascoside, vicine, zeatin, zeatin riboside, zeaxanthin, and zeinoxanthin are all found in bitter melon.
[00047] To date, close to 100 in vivo studies have demonstrated the blood sugar-lowering effect of this bitter fruit. The fruit has also shown the ability to enhance cells' uptake of glucose, to promote insulin release, and to potentiate the effect of insulin. In other in vivo studies, bitter melon fruit and/or seed has been shown to reduce total cholesterol. In one study, elevated cholesterol and triglyceride levels in diabetic rats were returned to normal after 10 weeks of treatment.
1000481 Several in vivo studies have demonstrated the antitumorous activity of the entire plant of bitter melon. In one study, a water extract blocked the growth of rat prostate carcinoma;
another study reported that a hot water extract of the entire plant inhibited the development of mammary tumors in mice. Numerous in vitro studies have also demonstrated the anticancerous and antileukemic activity of bitter melon against numerous cell lines, including liver cancer, human leukemia, melanoma, and solid sarcomas.
1000491 Bitter melon, like several of its isolated plant chemicals, also has been documented with in vitro antiviral activity against numerous viruses, including Epstein-Barr, herpes, and HIV viruses. In an in vivo study, a leaf extract increased resistance to viral infections and had an immunostimulant effect in humans and animals, increasing interferon production and natural killer cell activity.
[00050] In addition to these properties, leaf of bitter melon have demonstrated broad-spectrum antimicrobial activity. Various extracts of the leaves have demonstrated in vitro antibacterial activities against E. coli, Staphylococcus, Pseudomonas, Salmonella, Streptobacillus, and Streptococcus; an extract of the entire plant was shown to have antiprotozoal activity against Entamoeba histolytica. The fruit and fruit juice have demonstrated the same type of antibacterial properties and, in another study, a fruit extract demonstrated activity against the stomach ulcer-causing bacteria Helicobacterpylori.
1000511 Many in vivo clinical studies have demonstrated the relatively low toxicity of all parts of the bitter melon plant when ingested orally. However, toxicity and even death in laboratory animals has been reported when extracts are injected intravenously.
Other studies have shown extracts of the fruit and leaf (ingested orally) to be safe during pregnancy. The seeds, however, have demonstrated the ability to induce abortions in rats and mice, and the root has been documented as a uterine stimulant in animals. The fruit and leaf of bitter melon have demonstrated an in vivo antifertility effect in female animals; and in male animals, to affect the production of sperm negatively.
[00052] Over the years scientists have verified many of the traditional uses of this bitter plant that continues to be an important natural remedy in herbal medicine systems. Bitter melon capsules and tinctures are becoming more widely available in the United States and are employed by natural health practitioners for diabetes, viruses, colds and flu, cancer and tumors, high cholesterol, and psoriasis. Concentrated fruit and seed extracts can be found in capsules and tablets, as well as whole herb/vine powders and extracts in capsules and tinctures.
1000531 Bitter melon traditionally has been used as an abortive and has been documented with weak uterine stimulant activity; therefore, it is contraindicated during pregnancy.
[00054] This plant has been documented to reduce fertility in both males and females and should therefore not be used by those undergoing fertility treatment or seeking pregnancy.
1000551 The active chemicals in bitter melon can be transferred through breast milk;
therefore, it is contraindicated in women who are breast feeding.
[00056] All parts of bitter melon (especially the fruit and seed) have demonstrated in numerous in vivo studies that they lower blood sugar levels. As such, it is contraindicated in persons with hypoglycemia.
[00057] Although all parts of the plant have demonstrated active antibacterial activity, none have shown activity against fungi or yeast. Long-term use of this plant may result in the die-off of friendly bacteria with resulting opportunistic overgrowth of yeast (Candida). Cycling off the use of the plant (every 21-30 days for one week) may be warranted, and adding probiotics to the diet may be beneficial if this plant is used for longer than 30 days.
[00058] Bitter melon may potentiate insulin and anti-diabetic drugs and cholesterol-lowering drugs.
[00059] As stated before, Momordica charantia or commonly referred to as bitter melon has been one of the most extensively investigated and most widely acclaimed remedy for the treatment of diabetes since ancient time as all parts of the plant (fruit pulp, seed, leaves and whole plant) have shown hypoglycemic activity in normal animals, antihyperglycemic activity in alloxan or streptozotocin-induced diabetic animals and in genetic models of diabetes (Ahmed et al. 2001, Virdi et al. 2003 and Grover and Yadav 2004). Bitter melon has been observed to decrease serum glucose levels in animal experiments and in a few methodologically weak human studies as these investigations were neither randomized nor blinded and the dosage, toxicity and adverse effects have not been systematically assessed (Basch et al. 2003).
Nonetheless, the human, animal and in vitro evidence collectively suggests a moderate hypoglycemic effect of bitter melon.
[00060] A study by Akhtar et al. in 1981, investigated the effect of dried and powdered M.
charantia fruit on blood glucose level following oral administration to normal and alloxan-diabetic rabbits. Both normal and diabetic rabbits were randomly divided into 5 groups of six animals where group I served as a control whereas group II, III, IV and V were treated orally with 0.25, 0.5, 1.00 and 1.5 g/kg body weight of M. charantia powder suspended in 1%
carboxymethyl cellulose solution in water respectively. Blood was collected from an ear vein immediately after M. charantia administration at 5, 10 and 24 hour time intervals. There was no decrease in blood glucose at a dose of 0.25 g/kg in normal rabbits and at 0.25 and 0.5 g/kg in diabetic rabbits. The maximum glucose decrease was observed at 10 hours intervals in both normal and diabetic rabbits. A dose dependent decrease in blood glucose levels was observed at a dose of 1.0 and 1.5 g/kg in diabetic rabbits. The authors concluded that the whole dried powdered M. charantia fruit produced significant and consistent hypoglycemic effect in both normal and chemically induced insulin deficient rabbits.
[00061] In a study by Khanna et al. (1981), pharmacological trials on animals and clinical trials on humans were performed to investigate the effect of a hypoglycemic agent, polypeptide-p, isolated from the fruit, seeds and tissues of M. charantia. This active principle was actually isolated earlier by Khanna et al. in another study and was then called 'p-insulin' or 'v-insulin'.
The pharmacological trials in gerbils and langurs revealed that the polypeptide-p-ZnCIZ
administered subcutaneously was long acting and showed a significant blood-sugar-lowering effect. The clinical study also showed a hypoglycemic effect of polypeptide-p in juvenile and maturity-onset diabetic patients.
[00062] In a study by Leatherdale et al. (1981), the effect ofM. charantia on glucose and insulin concentrations was studied in non-insulin dependent diabetics and non-diabetic rats during a 50 g oral glucose tolerance test. Patients underwent three 50 g oral glucose tests: a standard test, a test with 50 mL ofjuice extracted from fresh M. charantia and a test after 8 - 11 weeks of consuming 0.23 kg of fried M. charantia daily. The rats were given 2 mL of the 10 mL
obtained from 100 g M. charantia. There was no associated increase in serum insulin response but blood glucose concentrations were significantly reduced in both patients and rats with the administration of raw juice whereas the daily supplement of fried M. charantia produced a small but significant improvement in glucose tolerance.
[00063] In a similar study by Welihinda et al. (1986), the hypoglycemic activity of M.
charantia was evaluated in non-insulin dependent maturity onset diabetics.
This study involved 18 patients with newly diagnosed type 2 diabetes mellitus. Each subject was given 100 mL of bitter melon juice 30 minutes before glucose loading for a glucose tolerance test (GTT). The results were compared to a GTT done on the previous day by each participant that showed significant improvements in GTT in 13 of the 18 participants (73%) after taking bitter melon.
The other 5 patients showed no significant improvements in their glucose tolerance. The authors explained that this may have been due to intra-individual variation which is normally seen in biological systems.
[00064] A study by Day et al. (1990), investigated the hypoglycemic effect of M.
charantia in normal mice by examining the plasma glucose and insulin responses to oral and intraperitoneal (i.p.) glucose tolerances and by examining different solvent-extracted fractions of M. charantia in streptozotocin diabetic mice. The hypoglycemic effect was evident at 60 minutes after oral glucose and 60 and 120 minutes after i.p. glucose at a dose of 1 g/mL. As in the experiment with the diabetic mice, oral administration of aqueous extract of M. charantia and residue after alkaline chloroform extraction reduced plasma glucose concentration within 1 hour also at a dose of lg/mL. Material recovered by acid water wash of the chloroform extract at a dose of 0.002g/mL produced a slowly generated hypoglycemic effect. Orally administered M.
charantia extracts lower glucose concentrations independently of intestinal glucose absorption and involves an extra-pancreatic action.
1000651 The hypoglycemic effects of fruit pulp, seed and whole plant of M.
charantia were studied in normal, IDDM and NIDDM model rats by Ali et al. in 1993.
Diabetes stimulating both IDDM and NIDDM were induced by i.p. injection of streptozotocin. The results indicated that the hypoglycemic principle is present only in the fruit pulp and that no blood glucose lowering effect was seen in either nonnal or diabetic (IDDM and NIDDM) rats when given seed extracts. It was noted that the fruit pulp extracts showed hypoglycemic activity in normal and NIDDM rats whereas no effect was produced in the IDDM model where 0 cells have been almost completely destroyed. An indication that the hypoglycemic effect of the active principle is probably mediated either by improving the insulin-secretory capacity of 0 cells or by improving the action of insulin 1000661 However, in a 2005 study by Sathishsekar and Subramanian, the conclusion of the study was that the administration of M. charantia seeds showed a hypoglycemic effect. The objective of the study was to examine the effect of aqueous extracts from seeds of two varieties of M. charantia on oxidative stress in plasma and the pancreas of streptozotocin-induced diabetic rats in comparison to a standard hypoglycemic drug, glibenclamide. Male albino rats of Wistar strain were divided into five groups of six animals in each group as follows:
normal control, diabetic control, diabetic treated with seed extract 1, diabetic treated with seed extract 2 and diabetic administered with glibenclamide. The duration of the experiment was 30 days and then the rats were sacrificed. The increase levels of blood glucose and decrease level of insulin in diabetic rats were normalized in M. charantia seed extract and glibenclamide treated diabetic rats. Also, the levels of thiobarbituric acid-reactive substances, lipid-hydroperoxides and reduced glutathione in both plasma and pancreas were significantly reversed to near normalcy after treatment. The levels of vitamin C and vitamin E in plasma and the activities of superoxide dismutase, catalase and glutathione peroxidase in pancreas were reversed to near normal levels and decreased activities respectively after M. charantia seed extract and glibenclamide treatment. Hence, controlling blood glucose level will thereby prevent the formation of free radicals or it may scavenge the reactive oxygen metabolites through various antioxidant compounds.
[00067] The antihyperglycemic effects of three extracts of fresh and dried whole M.
charantia fruit were studied by Virdi et al. in 2003 and compared to glibenclamide, a known synthetic drug. After 4 weeks of treatment at a dose of 20 mg/kg body weight, all three extract powders lowered blood glucose however the aqueous extract showed the maximum efficacy comparable to that of glibenclamide. This extract was further tested for nephrotoxicity, hepatotoxicity and biochemical parameters. No toxicity to liver and kidneys were shown based on histological and biochemical parameters. In conclusion, the aqueous extract powder of M.
charantia could be safely used in diabetic patients to control hyperglycemia and taken on a long term basis.
[00068] In 2001, Vikrant et al. carried out an experiment to study the effects of different doses of alcoholic and aqueous extracts of M. charantia on the metabolic parameters of fructose fed rats. Fructose feeding led to insulin resistance-hyperinsulinemia, hyperglycemia and slight elevation in serum triglycerides levels in which only aqueous extracts at the dose of 400 mg/day significantly prevented development of hyperglycemic as well as hyperinsulinemia.
Consequently, M. charantia might prove useful in the treatment and/or prevention of insulin resistance in non-diabetic state.
1000691 In a study by Shetty et al. in 2005, male Wistar rats were rendered diabetic by a single injection of streptozotocin such that there were two groups of 12 diabetic rats and two groups of 6 age-matched normal rats (control). Bitter gourd (M. charantia) was incorporated at 10% level in the diet and glycemic control of bitter gourd during diabetes was evaluated by monitoring diet intake, gain in body weight, water intake, urine sugar, urine volume, glomerular filtration rate and fasting blood glucose profiles. The administration of bitter gourd showed significant reduction in urine excretion, urine sugar excretion, glomerular filtration rate and fasting blood glucose level. At the end of the experiment, there was approximately 30%
improvement in the fasting blood glucose level and as such it is evident that bitter gourd is beneficial in controlling diabetes status.
[00070] In a study by Shibib et al. (1993), the biochemical mechanism of the hypoglycemic activity of M. charantia was examined in streptozotocin-induced diabetic rats.
The results of this study confirmed the hypoglycemic activity of M. charantia.
This activity was mediated through the suppression of hepatic gluconeogenic enzymes, glucose-6-phosphatase and fructose-1, 6-bisphophatase while stimulating glucose-6-phosphatse dehydrogenase. As such, M.
charantia is consistent with the antihyperglycemic effect reported in literature.
[00071] Most of the experimental studies reported in literature on the antihyperglycemic activity of M. charantia were induced by alloxan or streptozotocin. However, a study by Qakici et al. in 1994 examined the hypoglycemic effect of orally administrated extracts of M. charantia in normoglycemic or cyproheptadine-induced hyperglycemic mice. Streptozotocin or alloxan are known to cause irreversible destruction of insulin-secreting 0-cells in the islets of Langerhans in comparison to cyproheptadine which produces a reversible loss of pancreatic insulin when given in repeated doses. When fed orally, the aqueous extract of M. charantia but not the ethanolic extract showed anti-hyperglycemic and hypoglycemic effects in cyproheptadine-induced hyperglycemic and normoglycemic mice respectively.
1000721 A study undertaken by Sarkar et al. in 1996, demonstrated the hypoglycemic activity of the alcoholic extract of M. charantia in a validated animal model of diabetes mellitus known to respond to oral hypoglycemic drugs. The reduction in plasma glucose level was 10 -15% for M. charantia compared to a decrease of 40 - 44% for tolbutamide, a sulphonylurea drug, under similar conditions. Another finding was that repeated dosing of 500mg/kg of M.
charantia extract did not result in the deterioration of hypoglycemic response in normal rats. In diabetic rats, the oral glucose tolerance was improved causing a significant reduction in plasma glucose of 26% for M. charantia in comparison to metformin which caused a 40 -50%
reduction. The hypoglycemic activity of M. charantia is confirmed in both normal and diabetic animals as reported in the literature with similar responses from oral hypoglycemic drugs such as tolbutamide and metformin.
1000731 In a similar study by Miura et al. (2001), the hypoglycemic activity of the fruit of M. charantia was investigated in an animal model with type 2 diabetes with hyperinsulinemia.
After 3 weeks of oral administration of the water extract of M. charantia, the blood glucose and serum insulin levels were lowered. The results were supportive of the traditional medical use of M. charantia as an antidiabetic agent in type 2 diabetes.
[00074] In a follow up study, the effect of M. charantia with exercise on blood glucose was investigated as the treatment for type 2 diabetes (Miura et al. 2004).
Exercise therapy and diet are usually recommended for type 2 diabetics and as such the inclusion of exercise in this study is investigated. After 5 weeks of oral administration of the water extract of M. charantia fruit with exercise, blood glucose and insulin levels in diabetic rats were significantly reduced. It was lower than that of M. charantia supplementation only or exercise only. The hypoglycemic effect of M. charantia with exercise is a synergistic effect that is beneficial in type 2 diabetics.
[00075] The amount of research reported in literature on the beneficial effects of M.
charantia are mostly concentrated on its antidiabetic activity despite the possibility that it might affect lipid metabolism due to the interconnection between carbohydrate and lipid metabolism (Senanayake et al. 2004 (a)). People with diabetes mellitus are at a higher risk of developing heart disease and other blood vessel diseases as such there have been studies reporting hypertriglyceridaemia and hypercholesterolaemia in diabetic subjects (Chaturvedi 2005). There are a few experimental studies reported in literature that have examined the effect of M.
charantia on triglyceride and cholesterol levels in normal and chemically induced diabetic animals.
1000761 In a study by Jayasooriya et al. in 2000, the effects of dietary freeze-dried powdered bitter melon on serum glucose level and lipid parameters of serum and liver were examined in rats fed with and without cholesterol. Male Sprague-Dawley rats were fed the diets for 14 days at 0.5, 1 and 3% without added dietary cholesterol and at a level of 1% with or without added cholesterol and 0.15% bile acid. Dietary bitter melon consistently decreased serum glucose levels in rats fed cholesterol-free diets. The addition of bitter melon to cholesterol-free and cholesterol-enriched diets caused an elevated serum HDL-cholesterol level, an indication of antiatherogenic activity. Also, there was a consistent reduction of hepatic total cholesterol and triglyceride levels both in the presence and absence of dietary cholesterol where the reduction of triglyceride concentrations, in absence of dietary cholesterol, was in a dose-dependent manner. These results suggest that bitter melon contains components which influence the metabolism of serum and liver lipids such that it may improve and/or ameliorate lipid disorders such as hyperlipidemia and fatty liver.
[00077] In 2001, Ahmed et al. performed a study to investigate the long term effect of MC
fruit extract on blood plasma and tissue lipid profiles in normal and streptozotocin (STZ)--induced type 1 diabetic rats. Male Wistar rats were induced diabetic with a single intraperitoneal injection of a buffered solution of STZ at a dosage of 60 mg/kg body weight.
The animals were divided into four groups of six: diabetic, diabetic treated with karela extract, karela treated control and untreated control group. There was a significant increase in plasma non-esterified cholesterol, triglycerides and phospholipids in the diabetic rats accompanied by a decrease in HDL-cholesterol. However, over a 10-week treatment period with MC fruit extract, these levels returned close to normal. Also, under in vitro conditions, karela juice exhibited an inhibitory effect on membrane lipid peroxidation in a dose-dependant manner due to some antioxidant components present in the fruit extract. This study shows that besides its known hypoglycemic properties, karela fruit extract also exhibits strong hypolipidemic action on diabetic hypertriglyceridemia and hypercholesterolemia. Additionally, it has some antioxidative properties which contribute towards preventing lipid peroxidative damage.
1000781 In a study by Chen et al. (2003), the energy efficiency and adiposity of male rats were investigated with 0.375, 0.75 and 1.5% of bitter melon supplementations in high fat and low fat diets. Rats on the high fat diet with 1.5% bitter melon gained less weight and had less visceral fat than those fed the high fat diet. Bitter melon supplementation did not change apparent fat absorption but improved insulin resistance, lowered serum insulin and leptin but raised serum free fatty acid concentrations. The reduction of adiposity in rats fed a high fat diet indicates bitter melon has influences on lipid metabolism other than glucose metabolism.
1000791 Chen et al. carried out another study in 2005 to further investigate the metabolic consequences and possible mechanism(s) of the above study results. Bitter melon supplementation of 0.75 or 1.5% in either low-fat or high-fat diet had lower energy efficiency, visceral fat mass, plasma glucose and hepatic triacylglycerol but higher serum free fatty acids and plasnia catecholamines indicating an enhanced sympathetic activity and lipolytic process.
This clearly demonstrated the ability of bitter melon supplementation to reverse steatosis and normalize hepatic triacylgleycerol.
[00080] In a study by Senanayake et al. (2004 (b)), the effects of three different varieties of bitter melon on serum and liver lipids were examined. The effects on serum lipid parameters were marginal for all three varieties. On the other hand, all three varieties of bitter melon lowered hepatic triglyceride levels but the Koimidori variety was found to be the most effective.
Further investigation on this variety was carried out on finding the active component(s) of bitter melon responsible for liver triglyceride lowering activity by fractionation the bitter melon using organic solvents such as n-hexane, acetone, and methanol. The liver triglyceride levels in rats fed diets containing the methanol fraction at 1% level was similar to those fed unfractionated Koimidori at 3%. Therefore, the potent active component of bitter melon lowering liver triglyceride concentrations is found to be concentrated in the methanol fraction. The methanol fraction was able to lower liver cholesterol concentration in a dose-dependent manner. Hence, bitter melon is useful in relieving and/or ameliorating life style-related diseases such as fatty liver, hypertriglyceridemia and diabetes.
[00081] The authors from the above study carried out a very similar experiment using only the bitter melon of the Koimidori variety at levels of 0.5 and 1% to examine its hypolipidemic effect in Syrian hamsters fed a diet supplemented with and without 0.2%
cholesterol (Senanayake et al. 2004(a)). The serum triglyceride-lowering activity of dietary methanol fraction extracted from bitter melon was observed in a dose-dependent manner in hamsters fed diets with no added cholesterol. This dose-dependent triglyceride lowering effect was also seen in hamsters fed cholesterol-enriched diet supplemented with bitter melon. Even though elevated liver triglyceride levels were caused by the dietary cholesterol, these levels were still lower with bitter melon supplements. As a result, dietary bitter melon extract is effective in lowering serum and liver triglyceride especially in those with hypertriglyceridemia caused by dietary cholesterol.
1000821 In a more detailed study by Chaturvedi et al. (2004), the methanol extract of the fruit M. charantia was administered to diabetic rats to assess the long term effect of the extract on lipid profile and oral glucose tolerance test. After 30 days treatment, there was a significant reduction in triglyceride and LDL, and a significant increase in HDL level. A
significant effect on oral glucose tolerance was also noted but more obvious when the extract was given on the same day as the test.
1000831 In 2005, Chaturvedi performed a study to assess whether or not a methanol extract of M. charantia was able to normalize lipid and glucose levels in diabetic rats fed a high-fat and low-carbohydrate diet. Different doses of the extract were administered to alloxan-induced diabetic albino rats of the Horts Men strain for 45 days. Blood glucose, triglyceride, LDL and HDL levels showed a dose-dependent response to M. charantia extract while cholesterol levels were found to be significantly lower. M. charantia extract normalized blood glucose level, reduced triglyceride and LDL levels and increased HDL level. Hence, M.
charantia can play an active part in the management of diabetes and have a positive impact on factors responsible for heart diseases and other related disorders.
1000841 To date there have been no formal pharmacokinetic studies done on this plant in animals or humans. This may be due to the fact that they are commonly consumed as a vegetable. Hence, the absorption of bitter melon occurs in the intestinal tract. It is absorbed into the blood to affect glucose metabolism and incorporated into hepatic tissues to influence the metabolism of triglyceride (Jayasooriya et al. 2000 and Senanayake et al. 2004 (b)). The i i pharmacologic effects of the insulin-like polypeptide contained in bitter melon have an onset ction between 30 and 60 minutes and a peak effect at about four hours (Jellin et al. 2005).
[00085] The exact mechanism of action of Momordica charantia in animals and humans has not been elucidated; however investigators have proposed many plausible theories based on experimental results.
[00086] This effect seems to be through a number of different mechanisms. One of the earlier theory was that a component of bitter melon extract, polypeptide-p, have structural similarities to bovine insulin and as such the hypoglycemic activity (Khanna et al. 1981 and Basch et al. 2003). Other hypoglycemic chemicals of Momordica charantia include a mixture of steroidal saponins known as charantin, momordin Ic, oleanolic acid 3-0-monodesmoside and oleanolic acid 3-0-glucuronide (Grover and Yadav 2004). The mechanisms proposed for effects on glucose and insulin include an inhibitory effect on glucose absorption in the intestine by decreasing hepatic gluconeogenesis, increasing hepatic glycogen synthesis and increasing peripheral glucose oxidation (Shibib et al. 1993 and Basch et al. 2003), enhanced insulin release from beta cells (Sitasawad et al. 2000 and Saxena and Vikram 2004) and an extrapancreatic effect via increased glucose uptake by tissues and increased GLUT4 transporter protein of muscles (Day et al. 1990, Sarkar et al. 1996 and Miura et al. 2001).
[00087) The hypolipidemic effect of Momortica charantia has not been as extensively studied as the hypoglycemic effect; however, the mechanism of action that has been proposed by investigators based on experimental studies include controlling the hydrolysis of certain lipoproteins through enhanced sympathetic activity, lipolysis and possibly lipid oxidation, for selective uptake and metabolism by different tissues (Ahmed et al. 2001, Chen et al. 2003 and Chen and Li 2005), and bitter melon contains some active components, saponin and plant sterols that are known to have an inhibitory effect on lipid biosynthesis thus lowering liver triglyceride levels in animals and inhibiting cholesterol absorption in the intestinal tract (Senanayake et al.
2004 (a & b)). The strong antihyperlipidemic effect of M. charantia could also be explained through its control of hyperglycemia as insulin is a major determinant of total and very low density lipoprotein and triglyceride concentration (Ahmed et al. 2001). The hyperlipidemia observed in diabetics is a consequence of uninhibited action of lipolytic hormones on fat depots as insulin inhibits adipose tissue hormone-sensitive lipase reducing lipolysis and mobilization of peripheral depots (Ahmed et al. 2001).
[00088] Much literature has been published on bitter melon and cinnamon. A
partial listing of the published research on bitter melon is provided in Schedule A
and a partial listing of the published research on cinnamon is provided in Schedule B.
[00089] The present inventors have shown that the new therapeutic formulation comprising cinnamon and bitter melon demonstrates synergist activity and inter alia:
(a) healthy glucose level for people with type 2 diabetes;
(b) optimum level of cholesterol and triglycertides for people of all ages and thus reduces the risk of cardiovascular disease.
[00090] Thee new therapeutic formulation has also been proven as a powerful antioxidant and effective in helping to prevent cancer, heart disease, and stroke.
[00091] Another major benefit of the new therapeutic formulation is that it can prevent insulin resistance, a major and common complication that develops in people with type II
diabetes in later years.
[00092] The two main ingredients of the new therapeutic formulation come from cinnamon and bitter melon, two natural products with long history both as foods and as medicines. Both the ingredients have been successfully used as effective remedies for many medical conditions in Indian, Chinese and South American Traditional Medicine.
[00093] The mechanism of actions are different from one another as cinnamon activates the insulin kinase receptor to increase insulin sensitivity through insulin-mimetic activity while the mechanisms for bitter melon include increased insulin secretion, tissue glucose uptake, liver muscle glycogen synthesis, glucose oxidation and decreased hepatic gluconeogenesis. As a result, combining these two ingredients has a synergistic effect which would lead to greater benefits for people with diabetes. Also, it has been observed that people with diabetes are usually associated with hypertriglyceridemia and hypercholesterolemia.
Therefore, the combination of cinnamon and bitter melon has the potential to treat and prevent diabetes and other related cardiovascular diseases by lowering blood glucose levels and normalizing lipid profiles. Therefore, the combination of the medicinal ingredients is both novel and innovative.
[00094] The ratio of cinnamon to bitter melon may be varied and it is preferred that it be between sixty to seventy percent (60 - 70%) of cinnamon and forty to thirty percent (40 - 30%) of bitter melon.
1000951 One new therapeutic formulation contains cinnamon and bitter melon at a ratio of 60:40 which is the most synergistic combination of the two plants for the management of blood sugar levels of type 2 diabetes patients as well as for normalizing the lipid profiles. The new therapeutic formulation also contains the highest concentration of water soluble flavonoids extracted from cinnamon ( the part of the cinnamon extract responsible for its blood sugar lowering effect) compared to any other similar products in the market.
1000961 In order to achieve the desired synergism, the dosage of bitter melon should in the range of 100 to 200 milligrams two to three times a day with at least one gram of cinnamon per day. A particularly useful preparation is a 500 milligram capsule containing about 200 milligrams of bitter melon and 300 milligrams of cinnamon and one capsule should be taken twice a day to achieve the desired dosage.
[00097] Examples:
One particularly useful formulation is as follows:
Cinnamon (Cinnamomi cassiae: Cinnamonum verum) 280 mg Bitter melon (Momordica charantia) 120 mg Diluent 151 mg Lubricant 3 mg [00098] The bark of cinnamon was used in a ratio of 10:1 to produce the active ingredient.
Similarly, the whole melon was used in a ration of 10:1 to produce the desired amount of bitter melon. As the diluent, it was found useful to use microcrystalline cellulose in the amount of 150 milligrams mixed with one (1) milligram of dicalcium phosphate dihydrate.
Magnesium stearate was used as the lubricant. The ingredients were mixed and placed in a gelatin capsule.
Administration was also found to lower blood sugar levels and to normalize lipid profiles.
100991 One of the more difficult challenges for a manufacturer of a product which is orally ingested is to produce that product in a vehicle which encourages use of the product and which is attractive to the consumer. In this regard, the inventors have found that the new herbal product of the present invention may be incorporated into a vehicle which is chocolate based which would make the product much more palatable and attractive to the consumer.
[00100] In this regard, a product formulation has been invented which incorporates the novel herbal product into a vehicle comprised substantially of chocolate.
Although the product may be incorporated into any suitable chocolate vehicle, a particularly useful process and product is hereinafter described.
1001011 It has been found that certain chocolate form better vehicles than others. In particular, it is desired to use a sugar free chocolate formulation to avoid additional sugar in the final product.
[00102] The inventors have found the following four particularly useful formulations for the chocolate vehicle. Each of the following formulations do not contain any added sugar and are commercially available.
1001031 The first formulation is a dark chocolate which comprises forty-three percent (43%) maltitol, cocoa butter and cocoa powder processed with an alkali. A
chocolate liquor and cocoa powder along with milk fat and soya lecithin which is used as the emulsifier, and natural flavours are added.
[00104] A second formulation relates to a milk chocolate which contains maltitol in the amount of fifty-five percent (55%), cocoa butter and a chocolate liquor.
Calcium carbonate and milk fat are added as well as calcium caseinate and soya lecithin as the emulsifier with vanilla extract for taste.
[00105] A third useful formulation is a high protein sucrose free milk chocolate which includes maltitol, fractionated modified palm kernel oil, milk protein concentrate and cocoa powder. Calcium caseinate, soya lecithin as the emulsifier and vanilla extract are used.
[00106] The fourth formulation is a dark sugar free coating which is comprised of a chocolate liquor processed with an alkali, maltitol, cocoa butter, butter oil, soya lecithin as the emulsifier and vanilla extract.
[00107] The inventors have found the following process to be particularly useful.
[001081 The chocolate is first melted to a minimum temperature of ninety-five degrees Fahrenheit (95 F) to a maximum of one hundred and twenty degrees Fahrenheit (120 F).
Preferably, the chocolate is placed within a water jacketed kettle which has an agitator. After melting of the chocolate, the jacket is cooled to a temperature of sixty degrees Fahrenheit (60 F) to a maximum of ninety degrees Fahrenheit (90 F). The chocolate is allowed to cool to a minimum of sixty-eight degrees Fahrenheit (68 F) to a maximum of eight-nine degrees Fahrenheit (89 F) with the agitator running. The agitator continues to run until the chocolate starts to thicken.
[00109] After the chocolate has thickened, the jacket is gradually warmed to a temperature of a minimum of eighty degrees Fahrenheit (80 F) with the agitator running.
The chocolate is warmed to a temperature between eight-five degrees Fahrenheit (85 F) to ninety-five degrees Fahrenheit (95 F) with the agitator running and the herbal product is then added to this warmed chocolate in slow measures with the agitator running. The product is thoroughly mixed and when the mixing is completed, the jacket temperature is reduced. The chocolate is then poured into molds and cooled in a cooling tunnel.
1001101 It is preferred that the molds in which the chocolate is poured are kept at a temperature between seventy-eight degrees Fahrenheit (78 F) and eighty-two degrees Fahrenheit (82 F). The cooling tunnel subjects the chocolate in the mold to an initial cooling at a temperature between sixty-five degrees Fahrenheit (65 F) and seventy degrees Fahrenheit (70 F), to a main cooling stage between forty-five degrees Fahrenheit (45 F) to fifty degrees Fahrenheit (50 F) and to a final cooling stage of between sixty-five degrees Fahrenheit (65 F) to seventy degrees Fahrenheit (70 F).
[001111 It is preferred that for every forty (40) grams of chocolate, the product will contain between one hundred and fifty (150) milligrams to a maximum of one thousand (1000) milligrams of the cinnamon and to between one hundred (100) milligrams to one thousand (1000) milligrams of the bitter melon.
[00112] This produces an excellent product which finds wide acceptance with the consumer in view of the chocolate vehicle.
[00113] The inventors have also found that a more improved product can be produced when omega-3 fatty acids are added to the chocolate mix, preferably as a powder.
[001141 Omega-3 fatty acids are polyunsaturated fatty acids classified as essential because they cannot be synthesised in the body. Accordingly, they must be obtained from food. A good source of omega-3 fatty acids is fish oil. Essential fatty acids are essential to normal growth in young children and animals. A small amount of omega-3 fatty acids in the diet enables normal growth. It has now been found that there is a demonstrable link between omega-3 fatty acids and cancer protection. Further, it is known that omega-3 fatty acids significantly reduce blood triglyceride levels. Elevate triglyceride levels are associated with increased risk for cardiovascular disease, especially in women. Accordingly, it has been found that omega-3 fatty acids when introduced into the diet, will reduce high blood pressure and have an anti-inflammatory property.
1001151 Support can be found in the literature. For example, the following reference demonstrate the improved health effects of omega-3 fatty acids when introduced into the diet.
Suitable references include:
Robinson JG, Stone NJ. Antiatherosclerotic and antithrombotic effects of omega-3 fatty acids. Am J Cardiol. 2006 Aug 21;98(4A):39i-49i. Epub 2006 May 30. Review.
Psota TL, Gebauer SK, Kris-Etherton P. Dietary omega-3 fatty acid intake and cardiovascular risk. Am J Cardiol. 2006 Aug 21;98(4A):3i-18i. Epub 2006 May 30.
Review.
Hooper L, Thompson RL, Harrison RA, Summerbell CD, Ness AR, Moore HJ, Worthington HV, Durrington PN, Higgins JP, Capps NE, Riemersma RA, Ebrahim SB, Davey Smith G. Risks and benefits of omega-3 fats for mortality, cardiovascular disease, and cancer: systematic review. BMJ. 2006 Apr 1;332(7544):752-60. Epub 2006 Mar 24.
Review.
Shahidi F, Miraliakbari H. Omega-3 fatty acids in health and disease: part 2--health effects of omega-3 fatty acids in autoimmune diseases, mental health, and gene expression. J Med Food. 2005 Summer;8(2):133-48. Review 1001161 The human body can produce all but two of the fatty acids it needs.
The two fatty acids that the body cannot produce are widely distributed in fish oils. Since they cannot be made in the body from other substrates and must be supplied in food, they are called essential fatty acids. In the body, essential fatty acids are primarily used to produce hormone-like substances that regulate a wide range of functions, including blood pressure, blood clotting, blood lipid levels, the immune response and the inflammation response to injury infection.
1001171 Essential fatty acids are polyunsaturated fatty acids and are apparent compounds of, inter alia, omega-3 fatty acids. They are important in several human body systems including the immune system and in blood pressure regulation. They are used to make compounds such as prostaglandis the two most important long chain polyunsaturated fatty acids are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
[00118] Eicosapentaenoic acid (EPA) is an omega-3 essential fatty acid that acts as a precursor for prostaglandin-3 which inhibits patelet aggregation. It is commony found in fish oils from cod liver, herring, mackerel, salmon and sardine and it is also found in human breast milk. A large number of conditions in which EPA acts alone or with other omega-3 sources is thought to be effective including lowering inflammation.
[00119] Docosahexaenoic acid (DHA) is a major fatty acid in sperm and brain phospholipids, especially in the retina. Dietary DHA can reduce the level of blood triglycerides in humans, which may reduce the risk of heart disease. Low levels of DHA have been associated with Alzheimer's disease, depression and other diseases and there is evidence that DHA
supplementation may be effective in combating such diseases.
[00120] The omega-3 fatty acids is preferably supplied as a powder although there are forms which are available.
[00121] The novel product is made exactly as is the chocolate product using the same recipe except after the chocolate is fully added and mixed, then the omega-3 is added, preferably as a powder, immediately before the reduction of the jacket temperature. The amount of omega-3 added can vary between a minimum of 100 mg to a maximum of 1000 mg per 40 gm of final product.
[00122] Although the disclosure describes a preferred embodiment, the invention is not so limited. For a definition of the invention, reference is made to the claims.
SCHEDULE A
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U.S. Patents:
PAT. NO. Title 1 7,014,872 Herbal nutraceutical formulation for diabetics and process for preparing the same 2 6,964,786 Oil from Momordica charantia L., its method of preparation and uses 3 6,960,348 Goya derived cosmetic compositions for face and bodX
4 6,831,162 Protein/polypeptide-k obtained from Momordica charantia and a process for the extraction thereof 6,800,726 Proteins with increased levels of essential amino acids 6 6,770,585 Momordica cochinchinensis (Spreng.) .beta.-carotene and method 7 6,562,379 Adult-onset diabetes treatment method 8 6,379,718 Use of plant extracts for treatment of acne and furuncle 9 6,235,286 Adult-onset diabetes treatment method 6,183,747 Use of plant Momordica charactia extracts for treatment of acne acid 11 6,103,240 Herbal sweetening and preservative composition comprising licorice extract and mogrosides obtained from plants belonging to cucurbitaceae and/or momordica 12 5,942,233 Herbal composition for stimulating blood circulation 13 5,929,047 Anti-viral agent prepared by basic and acidic extraction of mangraves 14 5,900,240 Herbal compositions and their use as hypoglycemic agents 5,851,531 Adult-onset diabetes treatment method 16 5,484,889 Plant protein useful for treating tumors and HIV infection 17 4,368,149 Protein hybrid having c otoxicity and process for the preparation thereof 18 4,084,010 Glycosides having sweetness 1: Khan B, Arayne MS, Naz S, Mukhtar N.
Hypogylcemic activity of aqueous extract of some indigenous plants.
Pak J Pharm Sci. 2005 Jan;18(1):62-4.
PMID: 16431387 [PubMed - indexed for MEDLINE]
2: Reyes BA, Bautista ND, Tanquilut NC, Anunciado RV, Leung AB, Sanchez GC, Ma tg oto RL, Castronuevo P, Tsukamura H, Maeda KI.
Anti-diabetic potentials of Momordica charantia and Andrographis paniculata and their effects on estrous cyclicity of alloxan-induced diabetic rats.
J Ethnopharmacol. 2005 Nov 16; [Epub ahead of print]
PMID: 16298503 [PubMed - as supplied by publisher]
3: Ansari NM, Houlihan L, Hussain B, Pieroni A.
Antioxidant activity of five vegetables traditionally consumed by South-Asian migrants in Bradford, Yorkshire, UK.
Phytother Res. 2005 Oct;19(10):907-11.
PMID: 16261524 [PubMed - indexed for MEDLINE]
4: Yang X, Kong C, Liang W, Zhang M, Hu F.
[Relationships of Aulacophora beetles feeding behavior with cucurbitacin types in host crops]
Ying Yong Sheng Tai Xue Bao. 2005 Jul;16(7):1326-9. Chinese.
PMID: 16252877 [PubMed - in process]
5: Dengiz GO, Gursan N.
Effects of Momordica charantia L. (Cucurbitaceae) on indomethacin-induced ulcer model in rats.
Turk J Gastroenterol. 2005 Jun;16(2):85-88.
PMID: 16252198 [PubMed - as supplied by publisher]
6: Chan LL, Chen Q, Go AG, Lam EK, Li ET.
Reduced adiposity in bitter melon (Momordica charantia)-fed rats is associated with increased lipid oxidative enzyme activities and uncoupling protein expression.
J Nutr. 2005 Nov;135(11):2517-23.
PMID: 16251604 [PubMed - indexed for MEDLINE]
7: Shekelle PG, Hardy M, Morton SC, Coulter I, Venuturupalli S, Favreau J, Hilton LK.
Are Ayurvedic herbs for diabetes effective?
J Fam Pract. 2005 Oct;54(10):876-86. Review.
PMID: 16202376 [PubMed - indexed for MEDLINE]
8: Chaturvedi P.
Role of Momordica charantia in maintaining the normal levels of lipids and glucose in diabetic rats fed a high-fat and low-carbohydrate diet.
Br J Biomed Sci. 2005;62(3):124-6.
PMID: 16196458 [PubMed - indexed for MEDLINE]
9: Mekuria DB, Kashiwagi T, Tebayashi S, Kim CS.
Cucurbitane triterpenoid oviposition deterrent from Momordica charantia to the leafrniner, Liriomyza trifolii.
Biosci Biotechnol Biochem. 2005 Sep;69(9):1706-10.
PMID: 16195588 [PubMed - indexed for MEDLINE]
10: Girini MM, Ahamed RN, Aladakatti RH.
Effect of graded doses of Momordica charantia seed extract on rat sperm:
scanning electron microscope study.
J Basic Clin Physiol Pharmacol. 2005;16(1):53-66.
PMID: 16187486 [PubMed - indexed for MEDLINE]
11: Shetty AK, Kumar GS, Sambaiah K, Salimath PV.
Effect of bitter gourd (Momordica charantia) on glycaemic status in streptozotocin induced diabetic rats.
Plant Foods Hum Nutr. 2005 Sep;60(3):109-12.
PMID: 16187012 [PubMed - indexed for MEDLINE]
12: Hsieh CL, Lin YC, Ko WS, Peng CH, Huang CN, Peng RY.
Inhibitory effect of some selected nutraceutic herbs on LDL glycation induced by glucose and glyoxal.
J Ethnopharmacol. 2005 Dec 1;102(3):357-63. Epub 2005 Sep 12.
PMID: 16162395 [PubMed - indexed for MEDLINE]
13: Long-Yun L, Shu S, Wei YF, Zhong GY, Chen JH.
[Morphological and histological studies of Herpetospermum pedunculosum seeds and other substitutes]
Zhongguo Zhong Yao Za Zhi. 2005 Jul;30(14):1073-6. Chinese.
PMID: 16161440 [PubMed - in process]
14: Li LY, Deji LM, Wei YF, Zhong GY.
[Literature data investigation in semem of Herpetospermum pedunculosum]
Zhongguo Zhong Yao Za Zhi. 2005 Jun;30(12):893-5. Chinese.
PMID: 16124602 [PubMed - in process]
15: Zheng ZX, Teng JY, Liu JY, Qiu JH, Ouyang H, Xue C.
[The hypoglycemic effects of crude polysaccharides extract from Momordica charantia in mice]
Wei Sheng Yan Jiu. 2005 May;34(3):361-3. Chinese.
PMID: 16111053 [PubMed - in process]
16: Mutalik S, Chetana M, Sulochana B, Devi PU, Udupa N.
Effect of Dianex, a herbal formulation on experimentally induced diabetes mellitus.
Phytother Res. 2005 May;19(5):409-15.
PMID: 16106394 [PubMed - indexed for MEDLINE]
17: Akhtar S, Ali Khan A, Husain Q.
Partially purified bitter gourd (Momordica charantia) peroxidase catalyzed decolorization of textile and other industrially important dyes.
Bioresour Technol. 2005 Nov;96(16):1804-11. Epub 2005 Feb 25.
PMID: 16051087 [PubMed - indexed for MEDLINE]
18: Raj SK, Khan MS, Singh R, Kumari N, Prakash D.
Occurrence of yellow mosaic geminiviral disease on bitter gourd (Momordica charantia) and its impact on phytochemical contents.
Int J Food Sci Nutr. 2005 May;56(3):185-92.
PMID: 16009633 [PubMed - indexed for MEDLINE]
19: Kumar Shetty A, Suresh Kumar G, Veerayya Salimath P.
Bitter gourd (Momordica charantia) modulates activities of intestinal and renal disaccharidases in streptozotocin-induced diabetic rats.
Mol Nutr Food Res. 2005 Aug;49(8):791-6.
PMID: 16007724 [PubMed - indexed for MEDLINE]
20: Liu HL, Kong LY, Takaya Y, Niwa M.
Biotransformation of ferulic acid into two new dihydrotrimers by Momordica charantia peroxidase.
Chem Pharm Bull (Tokyo). 2005 Jul;53(7):816-9.
PMID: 15997142 [PubMed - indexed for MEDLINE
Biotransformation of ferulic acid into two new dihydrotrimers by Momordica charantia peroxidase.
Chem Pharm Bull (Tokyo). 2005 Jul;53(7):816-9.
PMID: 15997142 [PubMed - indexed for MEDLINE
21: Chen Q, Li ET.
Reduced adiposity in bitter melon (Momordica charantia) fed rats is associated with lower tissue triglyceride and higher plasma catecholamines.
Br J Nutr. 2005 May;93(5):747-54.
PMID: 15975176 [PubMed - indexed for MEDLINE]
Reduced adiposity in bitter melon (Momordica charantia) fed rats is associated with lower tissue triglyceride and higher plasma catecholamines.
Br J Nutr. 2005 May;93(5):747-54.
PMID: 15975176 [PubMed - indexed for MEDLINE]
22: Yasui Y, Hosokawa M, Sahara T, Suzuki R, Ohgiya S, Kohno H, Tanaka T, Miyashita K.
Bitter gourd seed fatty acid rich in 9c,11 t,13t-conjugated linolenic acid induces apoptosis and up-regulates the GADD45, p53 and PPARgamma in human colon cancer Caco-2 cells.
Prostaglandins Leukot Essent Fatty Acids. 2005 Aug;73(2):113-9.
PMID: 15961301 [PubMed - indexed for MEDLINE]
Bitter gourd seed fatty acid rich in 9c,11 t,13t-conjugated linolenic acid induces apoptosis and up-regulates the GADD45, p53 and PPARgamma in human colon cancer Caco-2 cells.
Prostaglandins Leukot Essent Fatty Acids. 2005 Aug;73(2):113-9.
PMID: 15961301 [PubMed - indexed for MEDLINE]
23: Ike K, Uchida Y, Nakamura T, Imai S.
Induction of interferon-gamma (IFN-gamma) and T helper 1(Thl) immune response by bitter gourd extract.
J Vet Med Sci. 2005 May;67(5):521-4.
PMID: 15942138 [PubMed - indexed for MEDLINE]
Induction of interferon-gamma (IFN-gamma) and T helper 1(Thl) immune response by bitter gourd extract.
J Vet Med Sci. 2005 May;67(5):521-4.
PMID: 15942138 [PubMed - indexed for MEDLINE]
24: Sathishsekar D, Subramanian S.
Beneficial effects of Momordica charantia seeds in the treatment of STZ-induced diabetes in experimental rats.
Biol Pharm Bull. 2005 Jun;28(6):978-83.
PMID: 15930730 [PubMed - indexed for MEDLINE]
Beneficial effects of Momordica charantia seeds in the treatment of STZ-induced diabetes in experimental rats.
Biol Pharm Bull. 2005 Jun;28(6):978-83.
PMID: 15930730 [PubMed - indexed for MEDLINE]
25: Sathishsekar D, Subramanian S.
Antioxidant properties of Momordica Charantia (bitter gourd) seeds on Streptozotocin induced diabetic rats.
Asia Pac J Clin Nutr. 2005;14(2):153-8.
PMID: 15927932 [PubMed - indexed for MEDLINE]
Antioxidant properties of Momordica Charantia (bitter gourd) seeds on Streptozotocin induced diabetic rats.
Asia Pac J Clin Nutr. 2005;14(2):153-8.
PMID: 15927932 [PubMed - indexed for MEDLINE]
26: Akhtar S, Khan AA, Husain Q.
Potential of immobilized bitter gourd (Momordica charantia) peroxidases in the decolorization and removal of textile dyes from polluted wastewater and dyeing effluent.
Chemosphere. 2005 Jul;60(3):291-301. Epub 2005 Jan 26.
PMID: 15924947 [PubMed - indexed for MEDLINE]
Potential of immobilized bitter gourd (Momordica charantia) peroxidases in the decolorization and removal of textile dyes from polluted wastewater and dyeing effluent.
Chemosphere. 2005 Jul;60(3):291-301. Epub 2005 Jan 26.
PMID: 15924947 [PubMed - indexed for MEDLINE]
27: Kimura Y, Akihisa T, Yuasa N, Ukiya M, Suzuki T, Toriyama M, Motohashi S, Tokuda H.
Cucurbitane-type triterpenoids from the fruit of Momordica charantia.
J Nat Prod. 2005 May;68(5):807-9.
PMID: 15921438 [PubMed - indexed for MEDLINE]
Cucurbitane-type triterpenoids from the fruit of Momordica charantia.
J Nat Prod. 2005 May;68(5):807-9.
PMID: 15921438 [PubMed - indexed for MEDLINE]
28: Sekar DS, Sivagnanam K, Subramanian S.
Antidiabetic activity of Momordica charantia seeds on streptozotocin induced diabetic rats.
Pharmazie. 2005 May;60(5):383-7.
PMID: 15918591 [PubMed - indexed for MEDLINE]
Antidiabetic activity of Momordica charantia seeds on streptozotocin induced diabetic rats.
Pharmazie. 2005 May;60(5):383-7.
PMID: 15918591 [PubMed - indexed for MEDLINE]
29: Sultan NA, SwamyMJ.
Energetics of carbohydrate binding to Momordica charantia (bitter gourd) lectin: an isothermal titration calorimetric study.
Arch Biochem Biophys. 2005 May 1;437(1):115-25.
PMID: 15820223 [PubMed - indexed for MEDLINE]
Energetics of carbohydrate binding to Momordica charantia (bitter gourd) lectin: an isothermal titration calorimetric study.
Arch Biochem Biophys. 2005 May 1;437(1):115-25.
PMID: 15820223 [PubMed - indexed for MEDLINE]
30: Nerurkar PV, Pearson L, Efird JT, Adeli K, Theriault AG, Nerurkar VR.
Microsomal triglyceride transfer protein gene expression and ApoB secretion are inhibited by bitter melon in HepG2 cells.
J Nutr. 2005 Apr;135(4):702-6.
PMID: 15795421 [PubMed - indexed for MEDLINE]
Microsomal triglyceride transfer protein gene expression and ApoB secretion are inhibited by bitter melon in HepG2 cells.
J Nutr. 2005 Apr;135(4):702-6.
PMID: 15795421 [PubMed - indexed for MEDLINE]
31: Yadav UC, Moorthy K, Baquer NZ.
Combined treatment of sodium orthovanadate and Momordica charantia fruit extract prevents alterations in lipid profile and lipogenic enzymes in alloxan diabetic rats.
Mol Cell Biochem. 2005 Jan;268(1-2):111-20.
PMID: 15724444 [PubMed - indexed for MEDLINE]
Combined treatment of sodium orthovanadate and Momordica charantia fruit extract prevents alterations in lipid profile and lipogenic enzymes in alloxan diabetic rats.
Mol Cell Biochem. 2005 Jan;268(1-2):111-20.
PMID: 15724444 [PubMed - indexed for MEDLINE]
32: Jantan I, Rafi IA, Jalil J.
Platelet-activating factor (PAF) receptor-binding antagonist activity of Malaysian medicinal plants.
Phytomedicine. 2005 Jan;12(1-2):88-92.
PMID: 15693713 [PubMed - indexed for MEDLINE]
Platelet-activating factor (PAF) receptor-binding antagonist activity of Malaysian medicinal plants.
Phytomedicine. 2005 Jan;12(1-2):88-92.
PMID: 15693713 [PubMed - indexed for MEDLINE]
33: Mahomoodally MF, Gurib-Fakim A, Subratty AH.
Experimental evidence for in vitro fluid transport in the presence of a traditional medicinal fruit extract across rat everted intestinal sacs.
Fundam Clin Pharmacol. 2005 Feb;19(1):87-92.
PMID: 15660964 [PubMed - indexed for MEDLINE]
Experimental evidence for in vitro fluid transport in the presence of a traditional medicinal fruit extract across rat everted intestinal sacs.
Fundam Clin Pharmacol. 2005 Feb;19(1):87-92.
PMID: 15660964 [PubMed - indexed for MEDLINE]
34: LNo authors listedl [Bitter melon to control high blood sugar]
Schweiz Rundsch Med Prax. 2004 Dec 8;93(50):2118. German. No abstract available.
PMID: 15646680 [PubMed - indexed for MEDLINE]
Schweiz Rundsch Med Prax. 2004 Dec 8;93(50):2118. German. No abstract available.
PMID: 15646680 [PubMed - indexed for MEDLINE]
35: Zhuang DH, Ouyang YC, Hu Z.
[Construction of prokaryotic expression vector for MAP30 gene and study of PCR
methods for rapid identification of recombinant.]
Yi Chuan. 2004 Sep;26(5):701-4. Chinese.
PMID: 15640088 [PubMed - indexed for MEDLINE]
[Construction of prokaryotic expression vector for MAP30 gene and study of PCR
methods for rapid identification of recombinant.]
Yi Chuan. 2004 Sep;26(5):701-4. Chinese.
PMID: 15640088 [PubMed - indexed for MEDLINE]
36: Ray SD, Lam TS, Rotollo JA, Phadke S, Patel C, Dontabhaktuni A, Mohammad S, Lee H, Strika S, Dobrogowska A, Bruculeri C, Chou A, Patel S, Patel R, Manolas T, Stohs S.
Oxidative stress is the master operator of drug and chemically-induced programmed and unprogrammed cell death: Implications of natural antioxidants in vivo.
Biofactors. 2004;21(1-4):223-32.
PMID: 15630201 [PubMed - indexed for MEDLINE]
Oxidative stress is the master operator of drug and chemically-induced programmed and unprogrammed cell death: Implications of natural antioxidants in vivo.
Biofactors. 2004;21(1-4):223-32.
PMID: 15630201 [PubMed - indexed for MEDLINE]
37: Schmourlo G, Mendonca-Filho RR, Alviano CS, Costa SS.
Screening of antifungal agents using ethanol precipitation and bioautography of medicinal and food plants.
J Ethnopharmacol. 2005 Jan 15;96(3):563-8. Epub 2004 Nov 25.
PMID: 15619579 [PubMed - indexed for MEDLINE]
Screening of antifungal agents using ethanol precipitation and bioautography of medicinal and food plants.
J Ethnopharmacol. 2005 Jan 15;96(3):563-8. Epub 2004 Nov 25.
PMID: 15619579 [PubMed - indexed for MEDLINE]
38: Chaturvedi P, George S, Milinganyo M, Tripathi YB.
Effect of Momordica charantia on lipid profile and oral glucose tolerance in diabetic rats.
Phytother Res. 2004 Nov;18(11):954-6.
PMID: 15597317 [PubMed - indexed for MEDLINE]
Effect of Momordica charantia on lipid profile and oral glucose tolerance in diabetic rats.
Phytother Res. 2004 Nov;18(11):954-6.
PMID: 15597317 [PubMed - indexed for MEDLINE]
39: Beloin N, Gbeassor M, Akpagana K, Hudson J, de Soussa K, Koumaglo K, Arnason JT.
Ethnomedicinal uses of Momordicacharantia (Cucurbitaceae) in Togo and relation to its phytochemistry and biological activity.
J Ethnopharmacol. 2005 Jan 4;96(1-2):49-55.
PMID: 15588650 [PubMed - indexed for MEDLINE]
Ethnomedicinal uses of Momordicacharantia (Cucurbitaceae) in Togo and relation to its phytochemistry and biological activity.
J Ethnopharmacol. 2005 Jan 4;96(1-2):49-55.
PMID: 15588650 [PubMed - indexed for MEDLINE]
40: Senanayake GV, Maruyama M, Sakono M, Fukuda N, Morishita T, Yukizaki C, Kawano M, Ohta H.
The effects of bitter melon (Momordica charantia) extracts on serum and liver lipid parameters in hamsters fed cholesterol-free and cholesterol-enriched diets.
J Nutr Sci Vitarninol (Tokyo). 2004 Aug;50(4):253-7.
PMID: 15527066 [PubMed - indexed for MEDLINE]
The effects of bitter melon (Momordica charantia) extracts on serum and liver lipid parameters in hamsters fed cholesterol-free and cholesterol-enriched diets.
J Nutr Sci Vitarninol (Tokyo). 2004 Aug;50(4):253-7.
PMID: 15527066 [PubMed - indexed for MEDLINE]
41: Babu PS, Stanely Mainzen Prince P.
Antihyperglycaemic and antioxidant effect of hyponidd, an ayurvedic herbomineral formulation in streptozotocin-induced diabetic rats.
J Pharm Pharmacol. 2004 Nov;56(11):1435-42.
PMID: 15525451 [PubMed - indexed for MEDLINE]
Antihyperglycaemic and antioxidant effect of hyponidd, an ayurvedic herbomineral formulation in streptozotocin-induced diabetic rats.
J Pharm Pharmacol. 2004 Nov;56(11):1435-42.
PMID: 15525451 [PubMed - indexed for MEDLINE]
42: ShengQ, Yao H, Xu H, Ling X, He T.
[Isolation of plant insulin from Momordica charantia seeds by gel filtration and RP-HPLC]
Zhong Yao Cai. 2004 Jun;27(6):414-6. Chinese.
PMID: 15524293 [PubMed - indexed for MEDLINE]
[Isolation of plant insulin from Momordica charantia seeds by gel filtration and RP-HPLC]
Zhong Yao Cai. 2004 Jun;27(6):414-6. Chinese.
PMID: 15524293 [PubMed - indexed for MEDLINE]
43: Tongia A, Tongia SK, Dave M.
Phytochemical determination and extraction of Momordica charantia fruit and its hypoglycemic potentiation of oral hypoglycemic drugs in diabetes mellitus (NIDDM).
Indian J Physiol Pharmacol. 2004 Apr;48(2):241-4.
PMID: 15521566 [PubMed - indexed for MEDLINE]
Phytochemical determination and extraction of Momordica charantia fruit and its hypoglycemic potentiation of oral hypoglycemic drugs in diabetes mellitus (NIDDM).
Indian J Physiol Pharmacol. 2004 Apr;48(2):241-4.
PMID: 15521566 [PubMed - indexed for MEDLINE]
44: Jagetia GC, Baliga MS.
The evaluation of nitric oxide scavenging activity of certain Indian medicinal plants in vitro:
a preliminary study.
J Med Food. 2004 Fa11;7(3):343-8.
PMID: 15383230 [PubMed - indexed for MEDLINE]
The evaluation of nitric oxide scavenging activity of certain Indian medicinal plants in vitro:
a preliminary study.
J Med Food. 2004 Fa11;7(3):343-8.
PMID: 15383230 [PubMed - indexed for MEDLINE]
45: Cummings E, Hundal HS, Wackerhage H, Hope M, Belle M, Adeghate E, Singh J.
Momordica charantia fruit juice stimulates glucose and amino acid uptakes in L6 myotubes.
Mol Cell Biochem. 2004 Jun;261(1-2):99-104.
PMID: 15362491 [PubMed - indexed for MEDLINE]
Momordica charantia fruit juice stimulates glucose and amino acid uptakes in L6 myotubes.
Mol Cell Biochem. 2004 Jun;261(1-2):99-104.
PMID: 15362491 [PubMed - indexed for MEDLINE]
46: Ahmed I, AdegLhate E, Cummings E, Sharma AK, Singh J.
Beneficial effects and mechanism of action of Momordica charantia juice in the treatment of streptozotocin-induced diabetes mellitus in rat.
Mol Cell Biochem. 2004 Jun;261(1-2):63-70.
PMID: 15362486 [PubMed - indexed for MEDLINE]
Beneficial effects and mechanism of action of Momordica charantia juice in the treatment of streptozotocin-induced diabetes mellitus in rat.
Mol Cell Biochem. 2004 Jun;261(1-2):63-70.
PMID: 15362486 [PubMed - indexed for MEDLINE]
47: Konishi T, Satsu H, Hatsugai Y, Aizawa K, Inakuma T, Nagata S, Sakuda SH, Na ag sawa H, Shimizu M.
Inhibitory effect of a bitter melon extract on the P-glycoprotein activity in intestinai Caco-2 cells.
Br J Pharmacol. 2004 Oct;143(3):379-87. Epub 2004 Sep 6.
PMID: 15351776 [PubMed - indexed for MEDLINE]
Inhibitory effect of a bitter melon extract on the P-glycoprotein activity in intestinai Caco-2 cells.
Br J Pharmacol. 2004 Oct;143(3):379-87. Epub 2004 Sep 6.
PMID: 15351776 [PubMed - indexed for MEDLINE]
48: Kimura K, Numata T, Kakuta Y, Kimura M.
Amino acids conserved at the C-terminal half of the ribonuclease T2 family contribute to protein stability of the enzymes.
Biosci Biotechnol Biochem. 2004 Aug;68(8):1748-57.
PMID: 15322360 [PubMed - indexed for MEDLINE]
Amino acids conserved at the C-terminal half of the ribonuclease T2 family contribute to protein stability of the enzymes.
Biosci Biotechnol Biochem. 2004 Aug;68(8):1748-57.
PMID: 15322360 [PubMed - indexed for MEDLINE]
49: Sultan NA, Maiya BG, Swamy MJ.
Thermodynamic analysis of porphyrin binding to Momordica charantia (bitter gourd) lectin.
Eur J Biochem. 2004 Aug;271(15):3274-82.
PMID: 15265047 [PubMed - indexed for MEDLINE]
Thermodynamic analysis of porphyrin binding to Momordica charantia (bitter gourd) lectin.
Eur J Biochem. 2004 Aug;271(15):3274-82.
PMID: 15265047 [PubMed - indexed for MEDLINE]
50: Limtrakul P, Khantamat 0, Pintha K.
Inhibition of P-glycoprotein activity and reversal of cancer multidrug resistance by Momordica charantia extract.
Cancer Chemother Pharmacol. 2004 Dec;54(6):525-30. Epub 2004 Jul 10.
PMID: 15248030 [PubMed - indexed for MEDLINE]
Inhibition of P-glycoprotein activity and reversal of cancer multidrug resistance by Momordica charantia extract.
Cancer Chemother Pharmacol. 2004 Dec;54(6):525-30. Epub 2004 Jul 10.
PMID: 15248030 [PubMed - indexed for MEDLINE]
51: McCarty MF.
Does bitter melon contain an activator of AMP-activated kinase?
Med Hypotheses. 2004;63(2):340-3.
PMID: 15236800 [PubMed - indexed for MEDLINE]
Does bitter melon contain an activator of AMP-activated kinase?
Med Hypotheses. 2004;63(2):340-3.
PMID: 15236800 [PubMed - indexed for MEDLINE]
52: Rotshtevn Y, Zito SW.
Application of modified in vitro screening procedure for identifying herbals possessing sulfonylurea-like activity.
J Ethnopharmacol. 2004 Aug;93(2-3):337-44.
PMID: 15234774 [PubMed - indexed for MEDLINE]
Application of modified in vitro screening procedure for identifying herbals possessing sulfonylurea-like activity.
J Ethnopharmacol. 2004 Aug;93(2-3):337-44.
PMID: 15234774 [PubMed - indexed for MEDLINE]
53: Deep G, Dasgupta T, Rao AR, Kale RK.
Cancer preventive potential of Momordica charantia L. against benzo(a)pyrene induced fore-stomach tumourigenesis in murine model system.
Indian J Exp Biol. 2004 Mar;42(3):319-22.
PMID: 15233304 [PubMed - indexed for MEDLINE]
Cancer preventive potential of Momordica charantia L. against benzo(a)pyrene induced fore-stomach tumourigenesis in murine model system.
Indian J Exp Biol. 2004 Mar;42(3):319-22.
PMID: 15233304 [PubMed - indexed for MEDLINE]
54: Prabakar K, Jebanesan A.
Larvicidal efficacy of some Cucurbitacious plant leaf extracts against Culex quinquefasciatus (Say).
Bioresour Technol. 2004 Oct;95(1):l 13-4.
PMID: 15207304 [PubMed - indexed for MEDLINE]
Larvicidal efficacy of some Cucurbitacious plant leaf extracts against Culex quinquefasciatus (Say).
Bioresour Technol. 2004 Oct;95(1):l 13-4.
PMID: 15207304 [PubMed - indexed for MEDLINE]
55: Grover JK, Yadav SP.
Pharmacological actions and potential uses of Momordica charantia: a review.
J Ethnopharmacol. 2004 Ju1;93(1):123-32. Review.
PMID: 15182917 [PubMed - indexed for MEDLINE]
Pharmacological actions and potential uses of Momordica charantia: a review.
J Ethnopharmacol. 2004 Ju1;93(1):123-32. Review.
PMID: 15182917 [PubMed - indexed for MEDLINE]
56 Kohno H, Suzuki R, Yasui Y, Hosokawa M, Miyashita K, Tanaka T.
Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats.
Cancer Sci. 2004 Jun;95(6):481-6.
PMID: 15182427 [PubMed - indexed for MEDLINE]
Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats.
Cancer Sci. 2004 Jun;95(6):481-6.
PMID: 15182427 [PubMed - indexed for MEDLINE]
57: Kohno H, Yasui Y, Suzuki R, Hosokawa M, Miyashita K, Tanaka T.
Dietary seed oil rich in conjugated linolenic acid from bitter melon inhibits azoxymethane-induced rat colon carcinogenesis through elevation of colonic PPARgamma expression and alteration of lipid composition.
Int J Cancer. 2004 Ju120;110(6):896-901.
PMID: 15170673 [PubMed - indexed for MEDLINE]
Dietary seed oil rich in conjugated linolenic acid from bitter melon inhibits azoxymethane-induced rat colon carcinogenesis through elevation of colonic PPARgamma expression and alteration of lipid composition.
Int J Cancer. 2004 Ju120;110(6):896-901.
PMID: 15170673 [PubMed - indexed for MEDLINE]
58: Saxena A, Vikram NK.
Role of selected Indian plants in management of type 2 diabetes: a review.
J Altern Complement Med. 2004 Apr;10(2):369-78. Review.
PMID: 15165418 [PubMed - indexed for MEDLINE]
Role of selected Indian plants in management of type 2 diabetes: a review.
J Altern Complement Med. 2004 Apr;10(2):369-78. Review.
PMID: 15165418 [PubMed - indexed for MEDLINE]
59: Shi M, ChengR.
[Effects of zinc and boron nutrition on balsam pear (Momordica charantia) yield and quality, and polyamines, hormone, and senescence of its leaves]
Ying Yong Sheng Tai Xue Bao. 2004 Jan;15(1):77-80. Chinese.
PMID: 15139192 [PubMed - indexed for MEDLINE]
[Effects of zinc and boron nutrition on balsam pear (Momordica charantia) yield and quality, and polyamines, hormone, and senescence of its leaves]
Ying Yong Sheng Tai Xue Bao. 2004 Jan;15(1):77-80. Chinese.
PMID: 15139192 [PubMed - indexed for MEDLINE]
60: Senanayake GV, Maruyama M, Shibuya K, Sakono M, Fukuda N, Morishita T, Yukizaki C, Kawano M, Ohta H.
effects of bitter melon (Momordica charantia) on serum and liver triglyceride levels in rats.
hnopharmacol. 2004 Apr;91(2-3):257-62.
[D: 15120448 [PubMed - indexed for MEDLINE]
effects of bitter melon (Momordica charantia) on serum and liver triglyceride levels in rats.
hnopharmacol. 2004 Apr;91(2-3):257-62.
[D: 15120448 [PubMed - indexed for MEDLINE]
61: Ichikawa M, Ohta M, Kanai S Yoshida Y, Takano S Ueoka T, Takahashi T, Kimoto K, Funakoshi A, Miyasaka K.
Bitter melon malt vinegar increases daily energy turnover in rats.
J Nutr Sci Vitaminol (Tokyo). 2003 Dec;49(6):428-33.
PMID: 14974734 [PubMed - indexed for MEDLINE]
Bitter melon malt vinegar increases daily energy turnover in rats.
J Nutr Sci Vitaminol (Tokyo). 2003 Dec;49(6):428-33.
PMID: 14974734 [PubMed - indexed for MEDLINE]
62: Lu L, Zhao Y.
[Study on hypoglycemic action and active constituents of Momordica charantia L.]
Zhong Yao Cai. 2002 Jun;25(6):449-51. Review. Chinese. No abstract available.
PMID: 14968781 [PubMed - indexed for MEDLINE]
[Study on hypoglycemic action and active constituents of Momordica charantia L.]
Zhong Yao Cai. 2002 Jun;25(6):449-51. Review. Chinese. No abstract available.
PMID: 14968781 [PubMed - indexed for MEDLINE]
63: Miura T, Itoh Y, Iwamoto N, Kato M, Ishida T.
Suppressive activity of the fruit of Momordica charantia with exercise on blood glucose in type 2 diabetic mice.
Biol Pharm Bull. 2004 Feb;27(2):248-50.
PMID: 14758046 [PubMed - indexed for MEDLINE]
Suppressive activity of the fruit of Momordica charantia with exercise on blood glucose in type 2 diabetic mice.
Biol Pharm Bull. 2004 Feb;27(2):248-50.
PMID: 14758046 [PubMed - indexed for MEDLINE]
64: Mahomoodally MF, Fakim AG, Subratty AH.
Momordica charantia extracts inhibit uptake of monosaccharide and amino acid across rat everted gut sacs in-vitro.
Biol Pharm Bull. 2004 Feb;27(2):216-8.
PMID: 14758036 [PubMed - indexed for MEDLINE]
Momordica charantia extracts inhibit uptake of monosaccharide and amino acid across rat everted gut sacs in-vitro.
Biol Pharm Bull. 2004 Feb;27(2):216-8.
PMID: 14758036 [PubMed - indexed for MEDLINE]
65: Liu X, Li S, Feng C, Yan D.
[Advances in the study of Momordica charantia L.]
Zhong Yao Cai. 2002 Mar;25(3):211-3. Review. Chinese. No abstract available.
PMID: 14748342 [PubMed - indexed for MEDLINE]
[Advances in the study of Momordica charantia L.]
Zhong Yao Cai. 2002 Mar;25(3):211-3. Review. Chinese. No abstract available.
PMID: 14748342 [PubMed - indexed for MEDLINE]
66: Manabe M, Takenaka R, Nakasa T, Okinaka O.
Induction of anti-inflammatory responses by dietary Momordica charantia L.
(bitter gourd).
Biosci Biotechnol Biochem. 2003 Dec;67(12):2512-7.
PMID: 14730127 [PubMed - indexed for MEDLINE]
Induction of anti-inflammatory responses by dietary Momordica charantia L.
(bitter gourd).
Biosci Biotechnol Biochem. 2003 Dec;67(12):2512-7.
PMID: 14730127 [PubMed - indexed for MEDLINE]
67: Raza H, Ahmed I, John A.
Tissue specific expression and immunohistochemical localization of glutathione S-transferase in streptozotocin induced diabetic rats: modulation by Momordica charantia (karela) extract.
Life Sci. 2004 Feb 6;74(12):1503-11.
PMID: 14729399 [PubMed - indexed for MEDLINE]
Tissue specific expression and immunohistochemical localization of glutathione S-transferase in streptozotocin induced diabetic rats: modulation by Momordica charantia (karela) extract.
Life Sci. 2004 Feb 6;74(12):1503-11.
PMID: 14729399 [PubMed - indexed for MEDLINE]
68: John AJ, Cherian R, Subhash HS, Cherian AM.
Evaluation of the efficacy of bitter gourd (momordica charantia) as an oral hypoglycemic agent--a randomized controlled clinical trial.
Indian J Physiol Pharmacol. 2003 Jul;47(3):363-5. No abstract available.
PMID: 14723327 [PubMed - indexed for MEDLINE]
Evaluation of the efficacy of bitter gourd (momordica charantia) as an oral hypoglycemic agent--a randomized controlled clinical trial.
Indian J Physiol Pharmacol. 2003 Jul;47(3):363-5. No abstract available.
PMID: 14723327 [PubMed - indexed for MEDLINE]
69: Chao CY, Huang CJ.
Bitter gourd (Momordica charantia) extract activates peroxisome proliferator-activated receptors and upregulates the expression of the acyl CoA oxidase gene in hepatoma cells.
J Biomed Sci. 2003 Nov-Dec;10(6 Pt 2):782-91.
PMID: 14631118 [PubMed - indexed for MEDLINE]
Bitter gourd (Momordica charantia) extract activates peroxisome proliferator-activated receptors and upregulates the expression of the acyl CoA oxidase gene in hepatoma cells.
J Biomed Sci. 2003 Nov-Dec;10(6 Pt 2):782-91.
PMID: 14631118 [PubMed - indexed for MEDLINE]
70: Ou L, Kong LY, Zhang XM, Niwa M.
Oxidation of ferulic acid by Momordica charantia peroxidase and related anti-inflammation activity changes.
Biol Pharm Bull. 2003 Nov;26(11):1511-6.
PMID: 14600392 [PubMed - indexed for MEDLINE]
Oxidation of ferulic acid by Momordica charantia peroxidase and related anti-inflammation activity changes.
Biol Pharm Bull. 2003 Nov;26(11):1511-6.
PMID: 14600392 [PubMed - indexed for MEDLINE]
71: Virdi J, Sivakami S, Shahani S, Suthar AC, Banavalikar MM, Biyani MK.
Antihyperglycemic effects of three extracts from Momordica charantia.
J Ethnopharmacol. 2003 Sep;88(1):107-11.
PMID: 12902059 [PubMed - indexed for MEDLINE]
Antihyperglycemic effects of three extracts from Momordica charantia.
J Ethnopharmacol. 2003 Sep;88(1):107-11.
PMID: 12902059 [PubMed - indexed for MEDLINE]
72: Telang M, Srinivasan A, Patankar A, Harsulkar A, Joshi V, Damle A, Deshpande V, Sainani M, Ranjekar P, Gupta G, Birah A, Rani S, Kachole M, Giri A, Gupta V.
Bitter gourd proteinase inhibitors: potential growth inhibitors of Helicoverpa armigera and Spodoptera litura.
Phytochemistry. 2003 Jul;63(6):643-52.
PMID: 12842136 [PubMed - indexed for MEDLINE]
Bitter gourd proteinase inhibitors: potential growth inhibitors of Helicoverpa armigera and Spodoptera litura.
Phytochemistry. 2003 Jul;63(6):643-52.
PMID: 12842136 [PubMed - indexed for MEDLINE]
73: Tao J, Zhong Z.
[Effects of light on morphological plasticity and biomass allocation of Momordica charantia]
Ying Yong Sheng Tai Xue Bao. 2003 Mar;14(3):336-40. Chinese.
PMID: 12836536 [PubMed - indexed for MEDLINE]
[Effects of light on morphological plasticity and biomass allocation of Momordica charantia]
Ying Yong Sheng Tai Xue Bao. 2003 Mar;14(3):336-40. Chinese.
PMID: 12836536 [PubMed - indexed for MEDLINE]
74: Pongnikom S, Fongmoon D, Kasinrerk W, Limtrakul PN.
Effect of bitter melon (Momordica charantia Linn) on level and function of natural killer cells in cervical cancer patients with radiotherapy.
J Med Assoc Thai. 2003 Jan;86(1):61-8.
PMID: 12678140 [PubMed - indexed for MEDLINE]
Effect of bitter melon (Momordica charantia Linn) on level and function of natural killer cells in cervical cancer patients with radiotherapy.
J Med Assoc Thai. 2003 Jan;86(1):61-8.
PMID: 12678140 [PubMed - indexed for MEDLINE]
75: Chen Q, Chan LL, Li ET.
Bitter melon (Momordica charantia) reduces adiposity, lowers serum insulin and normalizes glucose tolerance in rats fed a high fat diet.
J Nutr. 2003 Apr;133(4):1088-93.
PMID: 12672924 [PubMed - indexed for MEDLINE]
Bitter melon (Momordica charantia) reduces adiposity, lowers serum insulin and normalizes glucose tolerance in rats fed a high fat diet.
J Nutr. 2003 Apr;133(4):1088-93.
PMID: 12672924 [PubMed - indexed for MEDLINE]
76: Yeh GY, Eisenberg DM, Kaptchuk TJ, Phillips RS.
Systematic review of herbs and dietary supplements for glycemic control in diabetes.
Diabetes Care. 2003 Apr;26(4):1277-94. Review.
PMID: 12663610 [PubMed - indexed for MEDLINE]
Systematic review of herbs and dietary supplements for glycemic control in diabetes.
Diabetes Care. 2003 Apr;26(4):1277-94. Review.
PMID: 12663610 [PubMed - indexed for MEDLINE]
77: Xiao YH, Hou L, Yuan XH, Yang XY, Pei Y, Luo XY, Pei Y.
[Cloning and characterization of a homologous gene of plant class V chitinase from balsampear, Momordica charantia Linn.]
Yi Chuan Xue Bao. 2002;29(11):1028-33. Chinese.
PMID: 12645269 [PubMed - indexed for MEDLINE]
[Cloning and characterization of a homologous gene of plant class V chitinase from balsampear, Momordica charantia Linn.]
Yi Chuan Xue Bao. 2002;29(11):1028-33. Chinese.
PMID: 12645269 [PubMed - indexed for MEDLINE]
78: Grover JK, Rathi SS, Vats V.
Amelioration of experimental diabetic neuropathy and gastropathy in rats following oral administration of plant (Eugenia jambolana, Mucuna pruriens and Tinospora cordifolia) extracts.
Indian J Exp Biol. 2002 Mar;40(3):273-6.
PMID: 12635695 [PubMed - indexed for MEDLINE]
Amelioration of experimental diabetic neuropathy and gastropathy in rats following oral administration of plant (Eugenia jambolana, Mucuna pruriens and Tinospora cordifolia) extracts.
Indian J Exp Biol. 2002 Mar;40(3):273-6.
PMID: 12635695 [PubMed - indexed for MEDLINE]
79: Basch E, Gabardi S, Ulbricht C.
Bitter melon (Momordica charantia): a review of efficacy and safety.
Am J Health Syst Pharm. 2003 Feb 15;60(4):356-9. Review.
PMID: 12625217 [PubMed - indexed for MEDLINE]
Bitter melon (Momordica charantia): a review of efficacy and safety.
Am J Health Syst Pharm. 2003 Feb 15;60(4):356-9. Review.
PMID: 12625217 [PubMed - indexed for MEDLINE]
80: De S, Ganguly C, Das S.
Natural dietary agents can protect against DMBA genotoxicity in lymphocytes as revealed by single cell gel electrophoresis assay.
Teratog Carcinog Mutagen. 2003;Suppl 1:71-8.
PMID: 12616598 [PubMed - indexed for MEDLINE]
Natural dietary agents can protect against DMBA genotoxicity in lymphocytes as revealed by single cell gel electrophoresis assay.
Teratog Carcinog Mutagen. 2003;Suppl 1:71-8.
PMID: 12616598 [PubMed - indexed for MEDLINE]
81: Parvathi S, Kumar VJ.
Studies on chemical composition and utilization of the wild edible vegetable athalakkai (Momordica tuberosa).
Plant Foods Hum Nutr. 2002 Fal1;57(3-4):215-22.
PMID: 12602930 [PubMed - indexed for MEDLINE]
Studies on chemical composition and utilization of the wild edible vegetable athalakkai (Momordica tuberosa).
Plant Foods Hum Nutr. 2002 Fal1;57(3-4):215-22.
PMID: 12602930 [PubMed - indexed for MEDLINE]
82: Xie H, Huang S, Deng H, Wu Z, Ji A.
[Study on chemical components of Momordica charantia]
Zhong Yao Cai. 1998 Sep;21(9):458-9. Chinese.
PMID: 12569838 [PubMed - indexed for MEDLINE]
[Study on chemical components of Momordica charantia]
Zhong Yao Cai. 1998 Sep;21(9):458-9. Chinese.
PMID: 12569838 [PubMed - indexed for MEDLINE]
83: Lin X, Shen X, Long Z, Yang Q.
[Effects of cactus, alove veral, momorcica charantia on reducing the blood glucose of diabetic mice]
Wei Sheng Yan Jiu. 2001 Jul;30(4):203-5. Chinese.
PMID: 12561513 [PubMed - in process]
[Effects of cactus, alove veral, momorcica charantia on reducing the blood glucose of diabetic mice]
Wei Sheng Yan Jiu. 2001 Jul;30(4):203-5. Chinese.
PMID: 12561513 [PubMed - in process]
84: Kar A, Choudhary BK, Bandyopadhyay NG.
Comparative evaluation of hypoglycaemic activity of some Indian medicinal plants in alloxan diabetic rats.
J Ethnopharmacol. 2003 Jan;84(1):105-8.
PMID: 12499084 [PubMed - indexed for MEDLINE]
Comparative evaluation of hypoglycaemic activity of some Indian medicinal plants in alloxan diabetic rats.
J Ethnopharmacol. 2003 Jan;84(1):105-8.
PMID: 12499084 [PubMed - indexed for MEDLINE]
85: Rathi SS, Grover JK, Vikrant V, Biswas NR.
Prevention of experimental diabetic cataract by Indian Ayurvedic plant extracts.
Phytother Res. 2002 Dec;16(8):774-7.
PMID: 12458487 [PubMed - indexed for MEDLINE]
Prevention of experimental diabetic cataract by Indian Ayurvedic plant extracts.
Phytother Res. 2002 Dec;16(8):774-7.
PMID: 12458487 [PubMed - indexed for MEDLINE]
86: Huang CJ, Wu MC.
Differential effects of foods traditionally regarded as 'heating' and 'cooling' on prostaglandin E(2) production by a macrophage cell line.
J Biomed Sci. 2002 Nov-Dec;9(6 Pt 2):596-606.
PMID: 12432225 [PubMed - indexed for MEDLINE]
Differential effects of foods traditionally regarded as 'heating' and 'cooling' on prostaglandin E(2) production by a macrophage cell line.
J Biomed Sci. 2002 Nov-Dec;9(6 Pt 2):596-606.
PMID: 12432225 [PubMed - indexed for MEDLINE]
87: Nagasawa H, Watanabe K, Inatomi H.
Effects of bitter melon (Momordica charantia 1.) or ginger rhizome (Zingiber offifinale rosc) on spontaneous mammary tumorigenesis in SHN mice.
Am J Chin Med. 2002;30(2-3):195-205.
PMID: 12230008 [PubMed - indexed for MEDLINE]
Effects of bitter melon (Momordica charantia 1.) or ginger rhizome (Zingiber offifinale rosc) on spontaneous mammary tumorigenesis in SHN mice.
Am J Chin Med. 2002;30(2-3):195-205.
PMID: 12230008 [PubMed - indexed for MEDLINE]
88: Matsuur H, Asakawa C, Kurimoto M, Mizutani J.
Alpha-glucosidase inhibitor from the seeds of balsam pear (Momordica charantia) and the fruit bodies of Grifola frondosa.
Biosci Biotechnol Biochem. 2002 Jul;66(7):1576-8.
PMID: 12224646 [PubMed - indexed for MEDLINE]
Alpha-glucosidase inhibitor from the seeds of balsam pear (Momordica charantia) and the fruit bodies of Grifola frondosa.
Biosci Biotechnol Biochem. 2002 Jul;66(7):1576-8.
PMID: 12224646 [PubMed - indexed for MEDLINE]
89: Rathi SS, Grover JK, Vats V.
The effect of Momordica charantia and Mucuna pruriens in experimental diabetes and their effect on key metabolic enzymes involved in carbohydrate metabolism.
Phytother Res. 2002 May;16(3):236-43.
PMID: 12164268 [PubMed - indexed for MEDLINE]
The effect of Momordica charantia and Mucuna pruriens in experimental diabetes and their effect on key metabolic enzymes involved in carbohydrate metabolism.
Phytother Res. 2002 May;16(3):236-43.
PMID: 12164268 [PubMed - indexed for MEDLINE]
90: Li S, Zhang B, Deng H.
[Momordica charantia proteins against coxsackievirus B3 infection in vitro]
Hunan Yi Ke Da Xue Xue Bao. 1999;24(6):583-4. Chinese. No abstract available.
PMID: 12080730 [PubMed - indexed for MEDLINE]
[Momordica charantia proteins against coxsackievirus B3 infection in vitro]
Hunan Yi Ke Da Xue Xue Bao. 1999;24(6):583-4. Chinese. No abstract available.
PMID: 12080730 [PubMed - indexed for MEDLINE]
91: Kohler I Jenett-Siems K, Siems K, Hernandez MA, Ibarra RA, Berendsohn WG, Bienzle U, Eich E.
In vitro antiplasmodial investigation of medicinal plants from El Salvador.
Z Naturforsch [C]. 2002 Mar-Apr;57(3-4):277-81.
PMID: 12064726 [PubMed - indexed for MEDLINE]
In vitro antiplasmodial investigation of medicinal plants from El Salvador.
Z Naturforsch [C]. 2002 Mar-Apr;57(3-4):277-81.
PMID: 12064726 [PubMed - indexed for MEDLINE]
92: Grover JK, Yadav S, Vats V.
Medicinal plants of India with anti-diabetic potential.
J Ethnopharmacol. 2002 Jun;81(1):81-100. Review.
PMID: 12020931 [PubMed - indexed for MEDLINE]
Medicinal plants of India with anti-diabetic potential.
J Ethnopharmacol. 2002 Jun;81(1):81-100. Review.
PMID: 12020931 [PubMed - indexed for MEDLINE]
93: Parkash A, Ng TB, Tso WW.
Purification and characterization of charantin, a napin-like ribosome-inactivating peptide from bitter gourd (Momordica charantia) seeds.
J Pept Res. 2002 May;59(5):197-202.
PMID: 11966976 [PubMed - indexed for MEDLINE]
Purification and characterization of charantin, a napin-like ribosome-inactivating peptide from bitter gourd (Momordica charantia) seeds.
J Pept Res. 2002 May;59(5):197-202.
PMID: 11966976 [PubMed - indexed for MEDLINE]
94: Kohno H, Suzuki R, Noguchi R, Hosokawa M, Miyashita K, Tanaka T.
Dietary conjugated linolenic acid inhibits azoxymethane-induced colonic aberrant crypt foci in rats.
Jpn J Cancer Res. 2002 Feb;93(2):133-42.
PMID: 11856476 [PubMed - indexed for MEDLINE]
Dietary conjugated linolenic acid inhibits azoxymethane-induced colonic aberrant crypt foci in rats.
Jpn J Cancer Res. 2002 Feb;93(2):133-42.
PMID: 11856476 [PubMed - indexed for MEDLINE]
95: Miura T, Itoh C, Iwamoto N, Kato M, Kawai M, Park SR, Suzuki I.
Hypoglycemic activity of the fruit of the Momordica charantia in type 2 diabetic mice.
J Nutr Sci Vitaminol (Tokyo). 2001 Oct;47(5):340-4.
PMID: 11814149 [PubMed - indexed for MEDLINE]
Hypoglycemic activity of the fruit of the Momordica charantia in type 2 diabetic mice.
J Nutr Sci Vitaminol (Tokyo). 2001 Oct;47(5):340-4.
PMID: 11814149 [PubMed - indexed for MEDLINE]
96: Noguchi R, Yasui Y, Suzuki R, Hosokawa M, Fukunaga K, Miyashita K.
Dietary effects of bitter gourd oil on blood and liver lipids of rats.
Arch Biochem Biophys. 2001 Dec 15;396(2):207-12.
PMID: 11747298 [PubMed - indexed for MEDLINE]
Dietary effects of bitter gourd oil on blood and liver lipids of rats.
Arch Biochem Biophys. 2001 Dec 15;396(2):207-12.
PMID: 11747298 [PubMed - indexed for MEDLINE]
97: Numata T, Kimura M.
Contribution of Gln9 and Phe80 to substrate binding in ribonuclease MC 1 from bitter gourd seeds.
J Biochem (Tokyo). 2001 Nov;130(5):621-6.
PMID: 11686924 [PubMed - indexed for MEDLINE]
Contribution of Gln9 and Phe80 to substrate binding in ribonuclease MC 1 from bitter gourd seeds.
J Biochem (Tokyo). 2001 Nov;130(5):621-6.
PMID: 11686924 [PubMed - indexed for MEDLINE]
98: Wang HX, Ng TB.
Examination of lectins, polysaccharopeptide, polysaccharide, alkaloid, coumarin and trypsin inhibitors for inhibitory activity against human immunodeficiency virus reverse transcriptase and glycohydrolases.
Planta Med. 2001 Oct;67(7):669-72.
PMID: 11582548 [PubMed - indexed for MEDLINE]
Examination of lectins, polysaccharopeptide, polysaccharide, alkaloid, coumarin and trypsin inhibitors for inhibitory activity against human immunodeficiency virus reverse transcriptase and glycohydrolases.
Planta Med. 2001 Oct;67(7):669-72.
PMID: 11582548 [PubMed - indexed for MEDLINE]
99: Pari L, Ramakrishnan R, Venkateswaran S.
Antihyperglycaemic effect of Diamed, a herbal formulation, in experimental diabetes in rats.
J Pharm Pharmacol. 2001 Aug;53(8):1139-43.
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Antihyperglycaemic effect of Diamed, a herbal formulation, in experimental diabetes in rats.
J Pharm Pharmacol. 2001 Aug;53(8):1139-43.
PMID: 11518024 [PubMed - indexed for MEDLINE]
100: Jiratchariyakul W, Wiwat C, Vongsakul M, Somanabandhu A, Leelamanit W, Fujii I, Suwannaroj N, Ebizuka Y.
HIV inhibitor from Thai bitter gourd.
Planta Med. 2001 Jun;67(4):350-3.
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HIV inhibitor from Thai bitter gourd.
Planta Med. 2001 Jun;67(4):350-3.
PMID: 11458453 [PubMed - indexed for MEDLINE]
101: Grover JK, Vats V, Rathi SS, Dawar R.
Traditional Indian anti-diabetic plants attenuate progression of renal damage in streptozotocin induced diabetic mice.
J Ethnopharmacol. 2001 Aug;76(3):233-8.
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Traditional Indian anti-diabetic plants attenuate progression of renal damage in streptozotocin induced diabetic mice.
J Ethnopharmacol. 2001 Aug;76(3):233-8.
PMID: 11448544 [PubMed - indexed for MEDLINE]
102: Vikrant V, Grover JK, Tandon N, Rathi SS, Gupta N.
Treatment with extracts of Momordica charantia and Eugenia jambolana prevents hyperglycemia and hyperinsulinemia in fructose fed rats.
J Ethnopharmacol. 2001 Jul;76(2):139-43.
PMID: 11390126 [PubMed - indexed for MEDLINE]
Treatment with extracts of Momordica charantia and Eugenia jambolana prevents hyperglycemia and hyperinsulinemia in fructose fed rats.
J Ethnopharmacol. 2001 Jul;76(2):139-43.
PMID: 11390126 [PubMed - indexed for MEDLINE]
103: Chiampanichayakul S, Kataoka K, Arimochi H, Thumvijit S, Kuwahara T, Nakayama H, Vinitketkumnuen U, Ohnishi Y.
Inhibitory effects of bitter melon (Momordica charantia Linn.) on bacterial mutagenesis and aberrant crypt focus formation in the rat colon.
J Med Invest. 2001 Feb;48(1-2):88-96.
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Inhibitory effects of bitter melon (Momordica charantia Linn.) on bacterial mutagenesis and aberrant crypt focus formation in the rat colon.
J Med Invest. 2001 Feb;48(1-2):88-96.
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104: Ahmed I, Lakhani MS, Gillett M, John A, Raza H.
Hypotriglyceridemic and hypocholesterolemic effects of anti-diabetic Momordica charantia (karela) fruit extract in streptozotocin-induced diabetic rats.
Diabetes Res Clin Pract. 2001 Mar;51(3):155-61.
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Hypotriglyceridemic and hypocholesterolemic effects of anti-diabetic Momordica charantia (karela) fruit extract in streptozotocin-induced diabetic rats.
Diabetes Res Clin Pract. 2001 Mar;51(3):155-61.
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105: Araba BG.
Stimulation of protein biosynthesis in rat hepatocytes by extracts of Momordica charantia.
Phytother Res. 2001 Mar; 15(2):95-8.
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Stimulation of protein biosynthesis in rat hepatocytes by extracts of Momordica charantia.
Phytother Res. 2001 Mar; 15(2):95-8.
PMID: 11268104 [PubMed - indexed for MEDLINE]
106: Murakami T, Emoto A, Matsuda H, Yoshikawa M.
Medicinal foodstuffs. XXI. Structures of new cucurbitane-type triterpene glycosides, goyaglycosides-a, -b, -c, -d, -e, -f, -g, and -h, and new oleanane-type triterpene saponins, goyasaponins I, II, and III, from the fresh fruit of Japanese Momordica charantia L.
Chem Pharm Bull (Tokvo). 2001 Jan:49(1):54-63.
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Medicinal foodstuffs. XXI. Structures of new cucurbitane-type triterpene glycosides, goyaglycosides-a, -b, -c, -d, -e, -f, -g, and -h, and new oleanane-type triterpene saponins, goyasaponins I, II, and III, from the fresh fruit of Japanese Momordica charantia L.
Chem Pharm Bull (Tokvo). 2001 Jan:49(1):54-63.
PMID: 11201226 [PubMed - indexed for MEDLINE]
107: Numata T, Suzuki A, Yao M, Tanaka I, Kimura M.
Amino acid residues in ribonuclease MC 1 from bitter gourd seeds which are essential for uridine specificity.
Biochemistry. 2001 Jan 16;40(2):524-30.
PMID: 11148047 [PubMed - indexed for MEDLINE]
Amino acid residues in ribonuclease MC 1 from bitter gourd seeds which are essential for uridine specificity.
Biochemistry. 2001 Jan 16;40(2):524-30.
PMID: 11148047 [PubMed - indexed for MEDLINE]
108: Anila L, Vijayalakshmi NR.
Beneficial effects of flavonoids from Sesamum indicum, Emblica officinalis and Momordica charantia.
Phytother Res. 2000 Dec;14(8):592-5.
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Beneficial effects of flavonoids from Sesamum indicum, Emblica officinalis and Momordica charantia.
Phytother Res. 2000 Dec;14(8):592-5.
PMID: 11113993 [PubMed - indexed for MEDLINE]
109: Sitasawad SL, Shewade Y, Bhonde R.
Role of bittergourd fruit juice in stz-induced diabetic state in vivo and in vitro.
J Ethnopharmacol. 2000 Nov; 73 (1-2):71-9.
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Role of bittergourd fruit juice in stz-induced diabetic state in vivo and in vitro.
J Ethnopharmacol. 2000 Nov; 73 (1-2):71-9.
PMID: 11025141 [PubMed - indexed for MEDLINE]
110: Kamei K, Sato S, Hamato N, Takano R, Ohshima K, Yamamoto R, Nishino T, Kato H, Hara S.
Effect of P(2)' site tryptophan and P(20)' site deletion of Momordica charantia trypsin inhibitor lI on inhibition of proteinases.
Biochim Biophys Acta. 2000 Jul 14;1480(1-2):6-12.
PMID: 11004551 [PubMed - indexed for MEDLINE]
Effect of P(2)' site tryptophan and P(20)' site deletion of Momordica charantia trypsin inhibitor lI on inhibition of proteinases.
Biochim Biophys Acta. 2000 Jul 14;1480(1-2):6-12.
PMID: 11004551 [PubMed - indexed for MEDLINE]
111: Jayasooriya AP, Sakono M, Yukizaki C, Kawano M, Yamamoto K, Fukuda N.
Effects of Momordica charantia powder on serum glucose levels and various lipid parameters in rats fed with cholesterol-free and cholesterol-enriched diets.
J Ethnopharmacol. 2000 Sep;72(1-2):331-6.
PMID: 10967491 [PubMed - indexed for MEDLINE]
Effects of Momordica charantia powder on serum glucose levels and various lipid parameters in rats fed with cholesterol-free and cholesterol-enriched diets.
J Ethnopharmacol. 2000 Sep;72(1-2):331-6.
PMID: 10967491 [PubMed - indexed for MEDLINE]
112: Suzuki A, Yao M, Tanaka I Numata T, Kikukawa S Yamasaki N, Kimura M.
Crystal structures of the ribonuclease MC1 from bitter gourd seeds, complexed with 2'-UMP or 3'-UMP, reveal structural basis for uridine specificity.
Biochem Biophys Res Commun. 2000 Aug 28;275(2):572-6.
PMID: 10964705 [PubMed - indexed for MEDLINE]
Crystal structures of the ribonuclease MC1 from bitter gourd seeds, complexed with 2'-UMP or 3'-UMP, reveal structural basis for uridine specificity.
Biochem Biophys Res Commun. 2000 Aug 28;275(2):572-6.
PMID: 10964705 [PubMed - indexed for MEDLINE]
113: Ganguly C, De S, Das S.
Prevention of carcinogen-induced mouse skin papilloma by whole fruit aqueous extract of Momordica charantia.
Eur J Cancer Prev. 2000 Aug;9(4):283-8.
PMID: 10958332 [PubMed - indexed for MEDLINE]
Prevention of carcinogen-induced mouse skin papilloma by whole fruit aqueous extract of Momordica charantia.
Eur J Cancer Prev. 2000 Aug;9(4):283-8.
PMID: 10958332 [PubMed - indexed for MEDLINE]
114: Gurbuz I, Akyuz C, Yesilada E, Sener B.
Anti-ulcerogenic effect of Momordica charantia L. fruits on various ulcer models in rats. J
Ethnopharmacol. 2000 Jul;71(1-2):77-82.
PMID: 10904148 [PubMed - indexed for MEDLINE]
Anti-ulcerogenic effect of Momordica charantia L. fruits on various ulcer models in rats. J
Ethnopharmacol. 2000 Jul;71(1-2):77-82.
PMID: 10904148 [PubMed - indexed for MEDLINE]
115: Scartezzini P, Speroni E.
Review on some plants of Indian traditional medicine with antioxidant activity.
J Ethnopharmacol. 2000 Jul;71(1-2):23-43. Review.
PMID: 10904144 [PubMed - indexed for MEDLINE]
Review on some plants of Indian traditional medicine with antioxidant activity.
J Ethnopharmacol. 2000 Jul;71(1-2):23-43. Review.
PMID: 10904144 [PubMed - indexed for MEDLINE]
116: Lee-Huang S, Huang PL, Sun Y, Chen HC, Kung HF, Huang PL, Murphy WJ.
Inhibition of MDA-MB-231 human breast tumor xenografts and HER2 expression by anti-tumor agents GAP31 and MAP30.
Anticancer Res. 2000 Mar-Apr;20(2A):653-9.
PMID: 10810336 [PubMed - indexed for MEDLINE]
Inhibition of MDA-MB-231 human breast tumor xenografts and HER2 expression by anti-tumor agents GAP31 and MAP30.
Anticancer Res. 2000 Mar-Apr;20(2A):653-9.
PMID: 10810336 [PubMed - indexed for MEDLINE]
117: Numata T, Kashiba T, Hino M, Funatsu G, Ishiguro M, Yamasaki N, Kimura M.
Expression and mutational analysis of amino acid residues involved in catalytic activity in a ribonuclease MC 1 from the seeds of bitter gourd.
Biosci Biotechnol Biochem. 2000 Mar;64(3):603-5.
PMID: 10803962 [PubMed - indexed for MEDLINE]
Expression and mutational analysis of amino acid residues involved in catalytic activity in a ribonuclease MC 1 from the seeds of bitter gourd.
Biosci Biotechnol Biochem. 2000 Mar;64(3):603-5.
PMID: 10803962 [PubMed - indexed for MEDLINE]
118: Ahmad N, Hassan MR, Halder H, Bennoor KS.
Effect of Momordica charantia (Karolla) extracts on fasting and postprandial seruni glucose levels in NIDDM patients.
Bangladesh Med Res Counc Bull. 1999 Apr;25(1):l 1-3.
PMID: 10758656 [PubMed - indexed for MEDLINE]
Effect of Momordica charantia (Karolla) extracts on fasting and postprandial seruni glucose levels in NIDDM patients.
Bangladesh Med Res Counc Bull. 1999 Apr;25(1):l 1-3.
PMID: 10758656 [PubMed - indexed for MEDLINE]
119: Sato S, Kamei K, Taniguchi M, Sato H, Takano R, Mori H, Ichida M, Hara S.
Cloning and expression of the Momordica charantia trypsin inhibitor II gene in silkworm by using a baculovirus vector.
Biosci Biotechnol Biochem. 2000 Feb;64(2):393-8.
PMID: 10737198 [PubMed - indexed for MEDLINE]
Cloning and expression of the Momordica charantia trypsin inhibitor II gene in silkworm by using a baculovirus vector.
Biosci Biotechnol Biochem. 2000 Feb;64(2):393-8.
PMID: 10737198 [PubMed - indexed for MEDLINE]
120: Fong WP, Mock WY, Ng TB.
Intrinsic ribonuclease activities in ribonuclease and ribosome-inactivating proteins from the seeds of bitter gourd.
Int J Biochem Cell Biol. 2000 May;32(5):571-7.
PMID: 10736572 [PubMed - indexed for MEDLINE]
Intrinsic ribonuclease activities in ribonuclease and ribosome-inactivating proteins from the seeds of bitter gourd.
Int J Biochem Cell Biol. 2000 May;32(5):571-7.
PMID: 10736572 [PubMed - indexed for MEDLINE]
121: Raza H, Ahmed I, John A, Sharma AK.
Modulation of xenobiotic metabolism and oxidative stress in chronic streptozotocin-induced diabetic rats fed with Momordica charantia fruit extract.
J Biochem Mol Toxicol. 2000:14(3):131-9.
PMID: 10711628 [PubMed - indexed for MEDLINE]
Modulation of xenobiotic metabolism and oxidative stress in chronic streptozotocin-induced diabetic rats fed with Momordica charantia fruit extract.
J Biochem Mol Toxicol. 2000:14(3):131-9.
PMID: 10711628 [PubMed - indexed for MEDLINE]
122: Munoz V Sauvain M, Bourdy G, Callapa J, Rojas I, Vargas L, Tae A, Deharo E.
The search for natural bioactive compounds through a multidisciplinary approach in Bolivia. Part II. Antimalarial activity of some plants used by Mosetene indians.
J Ethnopharmacol. 2000 Feb;69(2):139-55.
PMID: 10687870 [PubMed - indexed for MEDLINE]
The search for natural bioactive compounds through a multidisciplinary approach in Bolivia. Part II. Antimalarial activity of some plants used by Mosetene indians.
J Ethnopharmacol. 2000 Feb;69(2):139-55.
PMID: 10687870 [PubMed - indexed for MEDLINE]
123: Cahoon EB, Carlson TJ, Ripp KG, Schweiger BJ, Cook GA, Hall SE, Kinney AJ.
Biosynthetic origin of conjugated double bonds: production of fatty acid components of high-value drying oils in transgenic soybean embryos.
Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12935-40.
PMID: 10536026 [PubMed - indexed for MEDLINE]
Biosynthetic origin of conjugated double bonds: production of fatty acid components of high-value drying oils in transgenic soybean embryos.
Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12935-40.
PMID: 10536026 [PubMed - indexed for MEDLINE]
124: Valbonesi P, Barbieri L, Bolognesi A, Bonora E, Polito L, Stirpe F.
Preparation of highly purified momordin II without ribonuclease activity.
Life Sci. 1999;65(14):1485-91.
PMID: 10530800 [PubMed - indexed for MEDLINE]
Preparation of highly purified momordin II without ribonuclease activity.
Life Sci. 1999;65(14):1485-91.
PMID: 10530800 [PubMed - indexed for MEDLINE]
125: Zhu Y, Huang Q, Qian M, Jia Y, Tang Y.
Crystal structure of the complex formed between bovine beta-trypsin and MCTI-A, a trypsin inhibitor of squash family, at 1.8-A resolution.
J Protein Chem. 1999 Jul;18(5):505-9.
PMID: 10524768 [PubMed - indexed for MEDLINE]
Crystal structure of the complex formed between bovine beta-trypsin and MCTI-A, a trypsin inhibitor of squash family, at 1.8-A resolution.
J Protein Chem. 1999 Jul;18(5):505-9.
PMID: 10524768 [PubMed - indexed for MEDLINE]
126: Schreiber CA, Wan L, Sun Y, Lu L, Krey LC, Lee-Huang S.
The antiviral agents, MAP30 and GAP31, are not toxic to human spermatozoa and may be useful in preventing the sexual transmission of human immunodeficiency virus type 1.
Fertil Steril. 1999 Oct;72(4):686-90.
PMID: 10521111 [PubMed - indexed for MEDLINE]
The antiviral agents, MAP30 and GAP31, are not toxic to human spermatozoa and may be useful in preventing the sexual transmission of human immunodeficiency virus type 1.
Fertil Steril. 1999 Oct;72(4):686-90.
PMID: 10521111 [PubMed - indexed for MEDLINE]
127: Yesilada E, Gurbuz I, Shibata H.
Screening of Turkish anti-ulcerogenic folk remedies for anti-Helicobacter pylori activity.
J Ethnopharmacol. 1999 Sep;66(3):289-93.
PMID: 10473175 [PubMed - indexed for MEDLINE]
Screening of Turkish anti-ulcerogenic folk remedies for anti-Helicobacter pylori activity.
J Ethnopharmacol. 1999 Sep;66(3):289-93.
PMID: 10473175 [PubMed - indexed for MEDLINE]
128: Zheng YT, Ben KL, Jin SW.
Alpha-momorcharin inhibits HIV-1 replication in acutely but not chronically infected T-lymphocytes.
Zhongguo Yao Li Xue Bao. 1999 Mar;20(3):239-43.
PMID: 10452099 [PubMed - indexed for MEDLINE]
Alpha-momorcharin inhibits HIV-1 replication in acutely but not chronically infected T-lymphocytes.
Zhongguo Yao Li Xue Bao. 1999 Mar;20(3):239-43.
PMID: 10452099 [PubMed - indexed for MEDLINE]
129: Nakagawa A, Tanaka I, Sakai R, Nakashima T, Funatsu G, Kimura M.
Crystal structure of a ribonuclease from the seeds of bitter gourd (Momordica charantia) at 1.75 A resolution.
Biochim BioDhvs Acta. 1999 Aua 17:1433(1-2):253-60.
PMID: 10446375 [PubMed - indexed for MEDLINE]
Crystal structure of a ribonuclease from the seeds of bitter gourd (Momordica charantia) at 1.75 A resolution.
Biochim BioDhvs Acta. 1999 Aua 17:1433(1-2):253-60.
PMID: 10446375 [PubMed - indexed for MEDLINE]
130: Huang B, Ng TB, Fong WP, Wan CC, Yeung HW.
Isolation of a trypsin inhibitor with deletion of N-terminal pentapeptide from the seeds of Momordica cochinchinensis, the Chinese drug mubiezhi.
Int J Biochem Cell Biol. 1999 Jun;31(6):707-15.
PMID: 10404643 [PubMed - indexed for MEDLINE]
Isolation of a trypsin inhibitor with deletion of N-terminal pentapeptide from the seeds of Momordica cochinchinensis, the Chinese drug mubiezhi.
Int J Biochem Cell Biol. 1999 Jun;31(6):707-15.
PMID: 10404643 [PubMed - indexed for MEDLINE]
131: Dhar P, Ghosh S, Bhattacharyya DK.
F~ Dietary effects of conjugated octadecatrienoic fatty acid (9 cis, 11 trans, 13 trans) levels on blood lipids and nonenzymatic in vitro lipid peroxidation in rats.
Lipids. 1999 Feb;34(2):109-14.
PMID: 10102236 [PubMed - indexed for MEDLINE]
F~ Dietary effects of conjugated octadecatrienoic fatty acid (9 cis, 11 trans, 13 trans) levels on blood lipids and nonenzymatic in vitro lipid peroxidation in rats.
Lipids. 1999 Feb;34(2):109-14.
PMID: 10102236 [PubMed - indexed for MEDLINE]
132: Frame AD, Rios-Olivares E, De Jesus L, Ortiz D, Pagan J, Mendez S.
Plants from Puerto Rico with anti-Mycobacterium tuberculosis properties.
P R Health Sci J. 1998 Sep;17(3):243-52.
PMID: 9883470 [PubMed - indexed for MEDLINE]
Plants from Puerto Rico with anti-Mycobacterium tuberculosis properties.
P R Health Sci J. 1998 Sep;17(3):243-52.
PMID: 9883470 [PubMed - indexed for MEDLINE]
133: Wang H, Ng TB.
Ribosome inactivating protein and lectin from bitter melon (Momordica charantia) seeds:
sequence comparison with related proteins.
Biochem Biophys Res Commun. 1998 Dec 9;253(1):143-6.
PMID: 9875234 [PubMed - indexed for MEDLINE]
Ribosome inactivating protein and lectin from bitter melon (Momordica charantia) seeds:
sequence comparison with related proteins.
Biochem Biophys Res Commun. 1998 Dec 9;253(1):143-6.
PMID: 9875234 [PubMed - indexed for MEDLINE]
134: Dhar P, Bhattacharyya DK.
Nutritional characteristics of oil containing conjugated octadecatrienoic fatty acid.
Ann Nutr Metab. 1998;42(5):290-6.
PMID: 9812020 [PubMed - indexed for MEDLINE]
Nutritional characteristics of oil containing conjugated octadecatrienoic fatty acid.
Ann Nutr Metab. 1998;42(5):290-6.
PMID: 9812020 [PubMed - indexed for MEDLINE]
135: Zanlbenedetti P, Giordano R, Zatta P.
Histochemical localization of glycoconjugates on microglial cells in Alzheimer's disease brain samples by using Abrus precatorius, Maackia amurensis, Momordica charantia, and Sambucus nigra lectins.
Exp Neurol. 1998 Sep;153(1):167-71.
PMID: 9743580 [PubMed - indexed for MEDLINE]
Histochemical localization of glycoconjugates on microglial cells in Alzheimer's disease brain samples by using Abrus precatorius, Maackia amurensis, Momordica charantia, and Sambucus nigra lectins.
Exp Neurol. 1998 Sep;153(1):167-71.
PMID: 9743580 [PubMed - indexed for MEDLINE]
136: Padma P, Komath SS, Swamy MJ.
Fluorescence quenching and time-resolved fluorescence studies on Momordica charantia (bitter gourd) seed lectin.
Biochem Mol Biol Int. 1998 Aug;45(5):911-22.
PMID: 9739456 [PubMed - indexed for MEDLINE]
Fluorescence quenching and time-resolved fluorescence studies on Momordica charantia (bitter gourd) seed lectin.
Biochem Mol Biol Int. 1998 Aug;45(5):911-22.
PMID: 9739456 [PubMed - indexed for MEDLINE]
137: Ahmed I, Adeghate E, Sharma AK, Pallot DJ, Singh J.
Effects of Momordica charantia fruit juice on islet morphology in the pancreas of the streptozotocin-diabetic rat.
Diabetes Res Clin Pract. 1998 Jun;40(3):145-51.
PMID: 9716917 [PubMed - indexed for MEDLINE]
Effects of Momordica charantia fruit juice on islet morphology in the pancreas of the streptozotocin-diabetic rat.
Diabetes Res Clin Pract. 1998 Jun;40(3):145-51.
PMID: 9716917 [PubMed - indexed for MEDLINE]
138: Naseem MZ, Patil SR, Patil SR, Ravindra, Patil RS.
Antispermatogenic and androgenic activities of Momordica charantia (Karela) in albino rats.
J Ethnopharmacol. 1998 May;61(1):9-16.
PMID: 9687077 [PubMed - indexed for MEDLINE]
Antispermatogenic and androgenic activities of Momordica charantia (Karela) in albino rats.
J Ethnopharmacol. 1998 May;61(1):9-16.
PMID: 9687077 [PubMed - indexed for MEDLINE]
139: Kusamran WR, Ratanavila A, Tepsuwan A.
Effects of neem flowers, Thai and Chinese bitter gourd fruits and sweet basil leaves on hepatic monooxygenases and glutathione S-transferase activities, and in vitro metabolic activation of chemical carcinogens in rats.
Food Chem Toxicol. 1998 Jun;36(6):475-84.
PMID: 9674955 [PubMed - indexed for MEDLINE]
Effects of neem flowers, Thai and Chinese bitter gourd fruits and sweet basil leaves on hepatic monooxygenases and glutathione S-transferase activities, and in vitro metabolic activation of chemical carcinogens in rats.
Food Chem Toxicol. 1998 Jun;36(6):475-84.
PMID: 9674955 [PubMed - indexed for MEDLINE]
140: Minami Y, Islam MR, Funatsu G.
Chemical modifications of momordin-a and luffin-a, ribosome-inactivating proteins from the seeds of Momordica charantia and Luffa cylindrica: involvement of His140, Tyr165, and Lys231 in the protein-synthesis inhibitory activity.
Biosci Biotechnol Biochem. 1998 May;62(5):959-64.
PMID: 9648227 [PubMed - indexed for MEDLINE]
Lans C, Brown G.
Observations on ethnoveterinary medicines in Trinidad and Tobago.
Prev Vet Med. 1998 May 1;35(2):125-42.
PMID: 9646336 [PubMed - indexed for MEDLINE]
142: Singh A, Singh SP, Bamezai R.
Momordica charantia (Bitter Gourd) peel, pulp, seed and whole fruit extract inhibits mouse skin papillomagenesis.
Toxicol Lett. 1998 Jan 16;94(1):37-46.
PMID: 9544697 [PubMed - indexed for MEDLINE]
143: Singh A, Singh SP, Bamezai R.
Postnatal efficacy of Momordica charantia peel, pulp, seed and whole fruit extract in the detoxication pathway of suckling neonates and lactating mice.
Cancer Lett. 1998 Jan 9;122(1-2):121-6.
PMID: 9464500 [PubMed - indexed for MEDLINE]
144: Liu L, Hammond EG, Nikolau BJ.
In Vivo Studies of the Biosynthesis of [alpha] -Eleostearic Acid in the Seed of Momordica charantia L.
Plant Physiol. 1997 Apr;113(4):1343-1349.
PMID: 12223677 [PubMed - as supplied by publisher]
145: Platel K, Srinivasan K.
Plant foods in the management of diabetes mellitus: vegetables as potential hypoglycaemic agents.
Nahrung. 1997 Apr;41(2):68-74. Review.
PMID: 9188186 [PubMed - indexed for MEDLINE]
146: Neumann GM, Condron R, Polya GM.
Purification and sequencing of napin-like protein small and large chains from Momordica charantia and Ricinus communis seeds and determination of sites phosphorylated by plant Ca(2+)-dependent protein kinase.
Biochim Biophys Acta. 1996 Dec 5;1298(2):223-40.
PMID: 8980648 [PubMed - indexed for MEDLINE]
147: Pu Z, Lu BY, Liu WY, Jin SW.
Characterization of the enzymatic mechanism of gamma-momorcharin, a novel ribosome-inactivating protein with lower molecular weight of 11,500 purified from the seeds of bitter gourd (Momordica charantia).
Biochem Biophys Res Commun. 1996 Dec 4;229(1):287-94.
PMID: 8954120 [PubMed - indexed for MEDLINE]
148: Omoregbe RE, Ikuebe OM, Ihimire IG.
Antimicrobial activity of some medicinal plants extracts on Escherichia coli, Salmonella paratyphi and Shigella dysenteriae.
Afr J Med Med Sci. 1996 Dec;25(4):373-5.
PMID: 9532310 [PubMed - indexed for MEDLINE]
149: Raza H, Ahmed I, Lakhani MS, Sharma AK, Pallot D, Monta ug e W.
Effect of bitter melon (Momordica charantia) fruit juice on the hepatic cytochrome P450-dependent monooxygenases and glutathione S-transferases in streptozotocin-induced diabetic rats.
Biochem Pharmacol. 1996 Nov 22;52(10):1639-42.
PMID: 8937480 [PubMed - indexed for MEDLINE]
150: Ueno HM, Doyama JT, Padovani CR, Salata E.
[Effect of Momordica charantia L. in mice infected with Plasmodium berghei]
Rev Soc Bras Med Trop. 1996 Sep-Oct;29(5):455-60. Portuguese.
PMID: 8966309 [PubMed - indexed for MEDLINE]
151: Ranios Ruiz A, De la Torre RA, Alonso N, Villaescusa A, Betancourt J, Vizoso A.
Screening of medicinal plants for induction of somatic segregation activity in Aspergillus nidulans.
J Ethnopharmacol. 1996 Ju15;52(3):123-7.
PMID: 8771452 [PubMed - indexed for MEDLINE]
152: Komath SS, Nadimpalli SK, Swamy MJ.
Purification in high yield and characterisation of the galactose-specific lectin from the seeds of snake gourd (Trichosanthes anguina).
Biochem Mol Biol Int. 1996 May;39(2):243-52.
PMID: 8799450 [PubMed - indexed for MEDLINE]
153: Bourinbaiar AS, Lee-Huang S.
The activity of plant-derived antiretroviral proteins MAP30 and GAP31 against herpes simplex virus in vitro.
Biochem Biophys Res Commun. 1996 Feb 27;219(3):923-9.
PMID: 8645280 [PubMed - indexed for MEDLINE]
154: Mock JW, Ng TB, Wong RN, Yao QZ, Yeung HW, Fong WP.
Demonstration of ribonuclease activity in the plant ribosome-inactivating proteins alpha-and beta-momorcharins.
Life Sci. 1996;59(22):1853-9.
PMID: 8950282 [PubMed - indexed for MEDLINE]
155: Basaran AA, Yu TW, Plewa MJ, Anderson D.
An investigation of some Turkish herbal medicines in Salmonella typhimurium and in the COMET assay in human lymphocytes.
Teratog Carcinog Mutagen. 1996;16(2):125-38.
PMID: 8875742 [PubMed - indexed for MEDLINE]
156: Sarkar S, Pranava M, Marita R.
Demonstration of the hypoglycemic action of Momordica charantia in a validated animal model of diabetes.
Pharmacol Res. 1996 Jan;33(1):1-4.
PMID: 8817639 [PubMed - indexed for MEDLINE]
157: Fong WP, Poon YT, Wong TM, Mock JW, Ng TB, Wong RN, Yao QZ, Yeung HW.
A highly efficient procedure for purifying the ribosome-inactivating proteins alpha- and beta-momorcharins from Momordica charantia seeds, N-terminal sequence comparison and establishment of their N-glycosidase activity.
Life Sci. 1996;59(11):901-9.
PMID: 8795701 [PubMed - indexed for MEDLINE]
158: Lee-Huang S Huang PL, Huang PL, Bourinbaiar AS, Chen HC, Kung HF.
Inhibition of the integrase of human immunodeficiency virus (HIV) type 1 by anti-HIV
plant proteins MAP30 and GAP3 1.
Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8818-22.
PMID: 7568024 [PubMed - indexed for MEDLINE]
159: Lee-Huang S Huang PL, Chen HC, Huang PL, Bourinbaiar A, Huang HI, Kung HF.
Anti-HIV and anti-tumor activities of recombinant MAP30 from bitter melon.
Gene. 1995 Aug 19;161(2):151-6.
PMID: 7665070 [PubMed - indexed for MEDLINE]
160: Arai K, Ishima R, Morikawa S Miyasaka A, Imoto T, Yoshimura S Aimoto S, Akasaka K.
Three-dimensional structure of gurmarin, a sweet taste-suppressing polypeptide.
J Biomol NMR. 1995 Apr;5(3):297-305.
PMID: 7787425 [PubMed - indexed for MEDLINE]
161:Bourinbaiar AS, Lee-Huang S.
Potentiation of anti-HIV activity of anti-inflammatory drugs, dexamethasone and indomethacin, by MAP30, the antiviral agent from bitter melon.
Biochem Biophys Res Commun. 1995 Mar 17;208(2):779-85.
PMID: 7695636 [PubMed - indexed for MEDLINE]
162: Miura S, Funatsu G.
Isolation and amino acid sequences of two trypsin inhibitors from the seeds of bitter gourd (Momordica charantia).
Biosci Biotechnol Biochem. 1995 Mar;59(3):469-73.
PMID: 7766185 [PubMed - indexed for MEDLINE]
163: Wu AM, Jiang YJ, Hwang PY, Shen FS.
Characterization of the okra mucilage by interaction with Gal, Ga1NAc and G1cNAc specific lectins.
Biochim Biophys Acta. 1995 Feb 23;1243(2):157-60.
PMID: 7873558 [PubMed - indexed for MEDLINE]
164: Hamato N, Koshiba T, Pham TN, Tatsumi Y, Nakamura D, Takano R, Hayashi K, Hong YM, Hara S.
Trypsin and elastase inhibitors from bitter gourd (Momordica charantia LINN.) seeds:
purification, amino acid sequences, and inhibitory activities of four new inhibitors.
J Biochem (Tokyo). 1995 Feb;117(2):432-7.
PMID: 7608135 [PubMed - indexed for MEDLINE]
165: Platel K, Srinivasan K.
Effect of dietary intake of freeze dried bitter gourd (Momordica charantia) in streptozotocin induced diabetic rats.
Nahrung. 1995;39(4):262-8.
PMID: 7477242 [PubMed - indexed for MEDLINE]
166: Hayashi K, Takehisa T, Hamato N Takano R, Hara S, Miyata T, Kato H.
Inhibition of serine proteases of the blood coagulation system by squash family protease inhibitors.
J Biochem (Tokyo). 1994 Nov;116(5):1013-18.
PMID: 7896727 [PubMed - indexed for MEDLINE]
167: Tennekoon KH, Jeevathayqparan S Angunawala P Karunanayake EH, Jayasin hg e KS.
Effect of Momordica charantia on key hepatic enzymes.
J Ethnopharmacol. 1994 Oct;44(2):93-7.
PMID: 7853870 [PubMed - indexed for MEDLINE]
168: Cakici I Hurmoglu C, Tunctan B, Abacioglu N, Kanzik I, Sener B.
Hypoglycaemic effect of Momordica charantia extracts in normoglycaemic or cyproheptadine-induced hyperglycaemic mice.
J Ethnopharmacol. 1994 Oct;44(2):117-21.
PMID: 7853862 [PubMed - indexed for MEDLINE]
169: Xiong JP, Xia ZX, Zhang L, Ye GJ, Jin SW, Wang Y.
Crystallization and preliminary crystallographic study of beta-momorcharin.
J Mol Biol. 1994 Apr 29;238(2):284-5.
PMID: 8158655 [PubMed - indexed for MEDLINE]
170: Husain J, Tickle IJ, Wood SP.
Crystal structure of momordin, a type I ribosome inactivating protein from the seeds of Momordica charantia.
FEBS Lett. 1994 Apr 4;342(2):154-8.
PMID: 8143869 [PubMed - indexed for MEDLINE]
171: Ng TB, Liu WK, Sze SF, Yeung HW.
Action of alpha-momorcharin, a ribosome inactivating protein, on cultured tumor cell lines.
Gen Pharmacol. 1994 Jan;25(1):75-7.
PMID: 8026716 [PubMed - indexed for MEDLINE]
172: Ali L, Khan AK, Mamun MI, Mosihuzzaman M, Nahar N, Nur-e-Alam M, Rokeya B.
Studies on hypoglycemic effects of fruit pulp, seed, and whole plant of Momordica charantia on normal and diabetic model rats.
Planta Med. 1993 Oct;59(5):408-12.
PMID: 8255932 [PubMed - indexed for MEDLINE]
173: Minami Y, Funatsu G.
The complete amino acid sequence of momordin-a, a ribosome-inactivating protein from the seeds of bitter gourd (Momordica charantia).
Biosci Biotechnol Biochem. 1993 Jul;57(7):l 141-4.
PMID: 7763984 [PubMed - indexed for MEDLINE]
174: Shibib BA, Khan LA, Rahman R.
Hypoglycaemic activity of Coccinia indica and Momordica charantia in diabetic rats:
depression of the hepatic gluconeogenic enzymes glucose-6-phosphatase and fructose-1,6-bisphosphatase and elevation of both liver and red-cell shunt enzyme glucose-6-phosphate dehydrogenase.
Biochem J. 1993 May 15;292 ( Pt 1):267-70.
PMID: 8389127 [PubMed - indexed for MEDLINE]
175: Porro G, Bolognesi A, Caretto P, Gromo G, Lento P, Mistza G, Sciumbata T, Stirpe F, Modena D.
In vitro and in vivo properties of an anti-CD5-momordin immunotoxin on normal and neoplastic T lymphocytes.
Cancer Immunol Immunother. 1993 May;36(5):346-50.
PMID: 7682894 [PubMed - indexed for MEDLINE]
176: Huang Q, Liu S, Tang Y.
Refined 1.6 A resolution crystal structure of the complex formed between porcine beta-trypsin and MCTI-A, a trypsin inhibitor of the squash family. Detailed comparison with bovine beta-trypsin and its complex.
J Mol Biol. 1993 Feb 20;229(4):1022-36.
PMID: 8445634 [PubMed - indexed for MEDLINE]
177: Platel K, Shurpalekar KS, Srinivasan K.
Influence of bitter gourd (Momordica charantia) on growth and blood constituents in albino rats.
Nahrung. 1993;37(2):156-60.
PMID: 8510714 [PubMed - indexed for MEDLINE]
178: De A, Funatsu G.
Crystallization and preliminary X-ray diffraction analysis of a plant ribonuclease from the seeds of the bitter gourd Momordica charantia.
J Mol Biol. 1992 Dec 20;228(4):1271-3.
PMID: 1474592 [PubMed - indexed for MEDLINE]
179: Higashino H, Suzuki A, Tanaka Y, Pootakham K.
[Hypoglycemic effects of Siamese Momordica charantia and Phyllanthus urinaria extracts in streptozotocin-induced diabetic rats (the lst report)]
Nippon Yakurigaku Zasshi. 1992 Nov;100(5):415-21. Japanese.
PMID: 1464400 [PubMed - indexed for MEDLINE]
180: Battelli MG, Montacuti V, Stirpe F.
High sensitivity of cultured human trophoblasts to ribosome-inactivating proteins.
Exp Cell Res. 1992 Jul;201(1):109-12.
PMID: 1612115 [PubMed - indexed for MEDLINE]
181: Ng TB, Chan WY, YeungHW.
Proteins with abortifacient, ribosome inactivating, immunomodulatory, antitumor and anti-AIDS activities from Cucurbitaceae plants.
Gen Pharmacol. 1992 Jul;23(4):579-90. Review.
PMID: 1397965 [PubMed - indexed for MEDLINE]
182: Huang Q, Liu S, Tang Y, Zeng F, Qian R.
Amino acid sequencing of a trypsin inhibitor by refined 1.6 A X-ray crystal structure of its complex with porcine beta-trypsin.
FEBS Lett. 1992 Feb 3;297(1-2):143-6.
PMID: 1551419 [PubMed - indexed for MEDLINE]
183: Omi T, Kamesaki T, Kajii E, Ikemoto S.
Method for detecting the lectin activity of Momordica charantia transferred from micro two-dimensional electrophoretic gel on to nitrocellulose.
J Chromatogr. 1991 Oct 4;570(2):399-405.
PMID: 1797856 [PubMed - indexed for MEDLINE]
184: Ogata F, Miyata T, Fuiii N, Yoshida N, Noda K, Makisumi S, Ito A.
Purification and amino acid sequence of a bitter gourd inhibitor against an acidic amino acid-specific endopeptidase of Streptomyces griseus.
J Biol Chem. 1991 Sep 5;266(25):16715-21.
PMID: 1679433 [PubMed - indexed for MEDLINE]
185: Ide H, Kimura M, Arai M, Funatsu G.
The complete amino acid sequence of ribonuclease from the seeds of bitter gourd (Momordica charantia).
FEBS Lett. 1991 Sep 2;289(l):126. No abstract available.
PMID: 1894001 [PubMed - indexed for MEDLINE]
186: Giron LM, Freire V, Alonzo A, Caceres A.
Ethnobotanical survey of the medicinal flora used by the Caribs of Guatemala.
J Ethnopharmacol. 1991 Sep;34(2-3):173-87.
PMID: 1795521 [PubMed - indexed for MEDLINE]
187: Kimura Y, Minami Y, Tokuda T, Nakajima S, Takagi S, Funatsu G.
Primary structures of N-linked oligosaccharides of momordin-a, a ribosome-inactivating protein from Momordica charantia seeds.
Agric Biol Chem. 1991 Aug;55(8):2031-6.
PMID: 1368729 [PubMed - indexed for MEDLINE]
188: Zafar R, Neerj a.
Momordica charantia--a review.
Hamdard Med. 1991 Jul-Sep;34(3):49-61. No abstract available.
PMID: 11613982 [PubMed - indexed for MEDLINE]
189: Yeung HW, Li WW, Ng TB.
Isolation of a ribosome-inactivating and abortifacient protein from seeds of Luffa acutangula.
Int J Pept Protein Res. 1991 Ju1;38(1):15-9.
PMID: 1938101 [PubMed - indexed for MEDLINE]
190: Ide H, Kimura M, Arai M, Funatsu G.
The complete amino acid sequence of ribonuclease from the seeds of bitter gourd (Momordica charantia).
FEBS Lett. 1991 Jun 24;284(2):161-4. Erratum in: FEBS Lett. 1991 Sep 2;289(1):126.
PMID: 2060635 [PubMed - indexed for MEDLINE]
191: Ho WK, Liu SC, Shaw PC, Yeung HW, Ng TB, Chan WY.
Cloning of the cDNA of alpha-momorcharin: a ribosome inactivating protein.
Biochim Biophys Acta. 1991 Feb 16;1088(2):311-4.
PMID: 2001404 [PubMed - indexed for MEDLINE]
192: Biswas AR, Ramaswamy S, Bapna JS.
Analgesic effect of Momordica charantia seed extract in mice and rats.
J Ethnopharmacol. 1991 Jan;31(1):115-8. No abstract available.
PMID: 2030591 [PubMed - indexed for MEDLINE]
193: Amorim CZ, Marques AD, Cordeiro RS.
Screening of the antimalarial activity of plants of the Cucurbitaceae family.
Mem Inst Oswaldo Cruz. 1991;86 Supp12:177-80.
PMID: 1841996 [PubMed - indexed for MEDLINE]
194: Lee-Huang S, Huang PL, Nara PL, Chen HC, Kung HF, HuangP, Huaniz HI, Huang PL.
MAP 30: a new inhibitor of HIV-1 infection and replication.
FEBS Lett. 1990 Oct 15;272(1-2):12-8.
PMID: 1699801 [PubMed - indexed for MEDLINE]
195: Day C, Cartwright T, Provost J, BaileY CJ.
Hypoglycaemic effect of Momordica charantia extracts.
Planta Med. 1990 Oct;56(5):426-9.
PMID: 2077547 [PubMed - indexed for MEDLINE]
196: Karunanayake EH, Jeevathayaparan S, Tennekoon KH.
Effect of Momordica charantia fruit juice on streptozotocin-induced diabetes in rats.
J Ethnopharmacol. 1990 Sep;30(2):199-204.
PMID: 2255210 [PubMed - indexed for MEDLINE]
197: Guevara AP, Lim-Sylianco C, Dayrit F, Finch P.
Antimutagens from Momordica charantia.
Mutat Res. 1990 Jun;230(2):121-6.
PMID: 2115617 [PubMed - indexed for MEDLINE]
198: Cunnick JE, Sakamoto K, Chapes SK, Fortner GW, Takemoto DJ.
Induction of tumor cytotoxic immune cells using a protein from the bitter melon (Momordica charantia).
Cell Immunol. 1990 Apr 1;126(2):278-89.
PMID: 2311123 [PubMed - indexed for MEDLINE]
199: Kamesaki T, Omi T, Kajii E, Ikemoto S.
New method of detecting the lectin activity of Momordica charantia.
Vox Sang. 1990;58(4):307-8. No abstract available.
PMID: 2399697 [PubMed - indexed for MEDLINE]
200: Zhu ZJ, Zhong ZC, Luo ZY, Xiao ZY.
[Studies on the active constituents of Momordica charantia L]
Yao Xue Xue Bao. 1990;25(12):898-903. Chinese.
PMID: 2104468 [PubMed - indexed for MEDLINE]
201: Chandrasekar B, Mukherjee B, Mukheriee SK.
Blood sugar lowering potentiality of selected Cucurbitaceae plants of Indian origin.
Indian J Med Res. 1989 Aug;90:300-5.
PMID: 2620957 [PubMed - indexed for MEDLINE]
202: Singh N, Tyagi SD, Agarwal SC.
Effects of long term feeding of acetone extract of Momordica charantia (whole fruit powder) on alloxan diabetic albino rats.
Indian J Physiol Pharmacol. 1989 Apr-Jun;33(2):97-100.
PMID: 2777367 [PubMed - indexed for MEDLINE]
203: Montecucchi PC, Lazzarini AM, Barbieri L, Stir_pe F, Soria M, Lappi D.
N-terminal sequence of some ribosome-inactivating proteins.
Int J Pept Protein Res. 1989 Apr;33(4):263-7.
PMID: 2753596 [PubMed - indexed for MEDLINE]
204: Hara S, Makino J, Ikenaka T.
Amino acid sequences and disulfide bridges of serine proteinase inhibitors from bitter gourd (Momordica charantia LINN.) seeds.
J Biochem (Tokyo). 1989 Jan;105(l):88-91.
PMID: 2738047 [PubMed - indexed for MEDLINE]
205: Ng TB, Li WW, Yeung HW.
Effects of lectins with various carbohydrate binding specificities on lipid metabolisni in isolated rat and hamster adipocytes.
Int J Biochem. 1989;21(2):149-55.
PMID: 2545472 [PubMed - indexed for MEDLINE]
206: Stirpe F, Wawrzynczak EJ, Brown AN, Knyba RE, Watson GJ, Barbieri L, Thorpe PE.
Selective cytotoxic activity of immunotoxins composed of a monoclonal anti-Thy 1.1 antibody and the ribosome-inactivating proteins bryodin and momordin.
Br J Cancer. 1988 Nov;58(5):558-61.
PMID: 3265330 [PubMed - indexed for MEDLINE]
207: Srivastava Y, Venkatakrishna-Bhatt H, Verma Y.
Effect of Momordica charantia Linn. pomous aqueous extract on cataractogenesis in murrin alloxan diabetics.
Pharmacol Res Commun. 1988 Mar;20(3):201-9.
PMID: 3387455 [PubMed - indexed for MEDLINE]
208: Yeung HW, Li WW, Feng Z, Barbieri L, Stirpe F.
Trichosanthin, alpha-momorcharin and beta-momorcharin: identity of abortifacient and ribosome-inactivating proteins.
Int J Pept Protein Res. 1988 Mar;31(3):265-8.
PMID: 3372132 [PubMed - indexed for MEDLINE]
209: Ng TB, Tam PP, Hon WK, Choi HL, Yeung HW.
Effects of momorcharins on ovarian response to gonadotropin-induced superovulation in mice.
Int J Fertil. 1988 Mar-Apr;33(2):123-8.
PMID: 2898450 [PubMed - indexed for MEDLINE]
210: Ng TB, Li WW, Yeung HW.
Effects of ginsenosides, lectins and Momordica charantia insulin-like peptide on corticosterone production by isolated rat adrenal cells.
J Ethnopharmacol. 1987 Sep-Oct;21(1):21-9.
PMID: 2826928 [PubMed - indexed for MEDLINE]
211: Srivastava Y, Venkatakrishna-Bhatt H, Verma Y, Prem AS.
Retardation of retinopathy by Momordica charantia L. (bitter gourd) fruit extract in alloxan diabetic rats.
Indian J Exp Biol. 1987 Aug;25(8):571-2. No abstract available.
PMID: 3446597 [PubMed - indexed for MEDLINE]
212: Leung SO, Yeung HW, Leung KN.
The immunosuppressive activities of two abortifacient proteins isolated from the seeds of bitter melon (Momordica charantia).
Immunopharmacology. 1987 Jun;13(3):159-71.
PMLD: 3497134 [PubMed - indexed for MEDLINE]
213: Ng TB, Wong CM, Li WW, Yeung HW.
Acid-ethanol extractable compounds from fruits and seeds of the bitter gourd Momordica charantia: effects on lipid metabolism in isolated rat adipocytes.
Am J Chin Med. 1987;15(1-2):31-42.
PMID: 3318384 [PubMed - indexed for MEDLINE]
214: Ng TB, Wong CM, Li WW, Yeung HW.
Peptides with antilipolytic and lipogenic activities from seeds of the bitter gourd Momordica charantia (family Cucurbitaceae).
Gen Pharmacol. 1987;18(3):275-81.
PMID: 3106137 [PubMed - indexed for MEDLINE]
215: Chan WY, Tam PP, Choi HL, Ng TB, Yeung HW.
Effects of momorcharins on the mouse embryo at the early organogenesis stage.
Contraception. 1986 Nov;34(5):537-44.
PMID: 3816236 [PubMed - indexed for MEDLINE]
216: Welihinda J, Karunanayake EH, Sheriff MH, Jayasinghe KS.
Effect of Momordica charantia on the glucose tolerance in maturity onset diabetes.
J Ethnopharmacol. 1986 Sep;17(3):277-82.
PMID: 3807390 [PubMed - indexed for MEDLINE]
217: Welihinda J, Karunanayake EH. , Extra-pancreatic effects of Momordica charantia in rats.
J Ethnopharmacol. 1986 Sep;17(3):247-55.
PMID: 3807387 [PubMed - indexed for MEDLINE]
218: Ng TB, Wong CM, Li WW, Yeung HW.
Isolation and characterization of a galactose binding lectin with insulinomimetic activities.
From the seeds of the bitter gourd Momordica charantia (Family Cucurbitaceae).
Int J Pept Protein Res. 1986 Aug;28(2):163-72.
PMID: 3533814 [PubMed - indexed for MEDLINE]
219: Ng TB, Wong CM, Li WW, Yeung HW.
A steryl glycoside fraction from Momordica charantia seeds with an inhibitory action on lipid metabolism in vitro.
Biochem Cell Biol. 1986 Aug;64(8):766-71.
PMID: 3021185 [PubMed - indexed for MEDLINE]
220: Ng TB, Wong CM, Li WW, Yeung HW.
Insulin-like molecules in Momordica charantia seeds.
J Ethnopharmacol. 1986 Jan;15(1):107-17.
PMID: 3520153 [PubMed - indexed for MEDLINE]
221: Wong CM, Yeung HW, Ng TB.
Screening of Trichosanthes kirilowii, Momordica charantia and Cucurbita maxima (family Cucurbitaceae) for compounds with antilipolytic activity.
J Ethnopharmacol. 1985 Jul;13(3):313-21.
PMID: 4058034 [PubMed - indexed for MEDLINE]
222: Lappi DA, Esch FS, Barbieri L, Stirpe F, Soria M.
Characterization of a Saponaria officinalis seed ribosome-inactivating protein:
immunoreactivity and sequence homologies.
Biochem Biophys Res Commun. 1985 Jun 28;129(3):934-42.
PMID: 3925952 [PubMed - indexed for MEDLINE]
223: Lei QJ, Jiang XM, Luo AC, Liu ZF, He XC, Wang XD, Cui FY, Chen PX.
Influence of balsam pear (the fruit of Momordica charantia L.) on blood sugar level.
J Tradit Chin Med. 1985 Jun;5(2):99-106. No abstract available.
PMID: 3851122 [PubMed - indexed for MEDLINE]
224: Bailey CJ, Day C, Turner SL, Leatherdale BA.
Cerasee, a traditional treatment for diabetes. Studies in normal and streptozotocin diabetic mice.
Diabetes Res. 1985 Mar;2(2):81-4.
PMID: 3899464 [PubMed - indexed for MEDLINE]
225: Meir P, Yaniv Z.
An in vitro study on the effect of Momordica charantia on glucose uptake and glucose metabolism in rats.
Planta Med. 1985 Feb;(1):12-6. No abstract available.
PMID: 4011748 [PubMed - indexed for MEDLINE]
226: Chan WY, Tam PP, So KC, Yeung HW.
The inhibitory effects of beta-momorcharin on endometrial cells in the mouse.
Contraception. 1985 Jan;31(1):83-90.
PMID: 3987275 [PubMed - indexed for MEDLINE]
227: Karunanayake EH, Welihinda J, Sirimanne SR, Sinnadorai G.
Oral hypoglycaemic activity of some medicinal plants of Sri Lanka.
J Etlinopharmacol. 1984 Jul;11(2):223-31.
PMID: 6492834 [PubMed - indexed for MEDLINE]
228: Foxwell B, Long J, Stiipe F.
Cytoxicity of erythrocyte ghosts loaded with ribosome-inactivating proteins following fusion with CHO cells.
Biochem Int. 1984 Jun;8(6):811-9.
PMID: 6541045 [PubMed - indexed for MEDLINE]
229: Chan WY, Tam PP, Yeung HW.
The termination of early pregnancy in the mouse by beta-momorcharin.
Contraception. 1984 Jan;29(1):91-100.
PMID: 6734206 [PubMed - indexed for MEDLINE]
230: Jilka C, Strifler B, Fortner GW, Hays EF, Takemoto DJ.
In vivo antitumor activity of the bitter melon (Momordica charantia).
Cancer Res. 1983 Nov;43(11):5151-5.
PMID: 6616452 [PubMed - indexed for MEDLINE]
231: Sargiacomo M, Barbieri L, Stirpe F, Tomasi M.
Cytotoxicity acquired by ribosome-inactivating proteins carried by reconstituted Sendai virus envelopes.
FEBS Lett. 1983 Jun 27;157(1):150-4.
PMID: 6305714 [PubMed - indexed for MEDLINE]
232: Spreafico F, Malfiore C, Moras ML, Marmonti L, Filippeschi S, Barbieri L, Perocco P, Stirpe F.
The immunomodulatory activity of the plant proteins Momordica charantia inhibitor and pokeweed antiviral protein.
Int J Immunopharmacol. 1983;5(4):335-43.
PMID: 6629594 [PubMed - indexed for MEDLINE]
233: Takemoto DJ, Jilka C, Rockenbach S, Hu heg s JV.
Purification and characterization of a cytostatic factor with anti-viral activity from the bitter melon.
Prep Biochem. 1983;13(4):371-93.
PMID: 6196772 [PubMed - indexed for MEDLINE]
234: Takemoto DJ, Jilka C, Rockenbach S, Hughes JV.
Purification and characterization of a cytostatic factor with anti-viral activity from the bitter melon.
Prep Biochem. 1983;13(5):397-421.
PMID: 6142453 [PubMed - indexed for MEDLINE]
235: Falasca A, Gasperi-Campani A, Abbondanza A, Barbieri L, Stirpe F.
Properties of the ribosome-inactivating proteins gelonin, Momordica charantia inhibitor, and dianthins.
Biochem J. 1982 Dec 1;207(3):505-9.
PMID: 6819861 [PubMed - indexed for MEDLINE]
236: Farnsworth NR, Waller DP.
Current status of plant products reported to inhibit sperm.
Res Front Fertil Regul. 1982 Jun;2(1):1-16.
PMID: 12179631 [PubMed - indexed for MEDLINE]
237: Akhtar MS.
Trial of Momordica charantia Linn (Karela) powder in patients with maturity-onset diabetes.
J Pak Med Assoc. 1982 Apr;32(4):106-7. No abstract available.
PMID: 6806502 [PubMed - indexed for MEDLINE]
238: Kedar P, Chakrabarti CH.
Effects of bittergourd (Momordica charantia) seed & glibenclamide in streptozotocin induced diabetes mellitus.
Indian J Exp Biol. 1982 Mar;20(3):232-5. No abstract available.
PMID: 6811427 [PubMed - indexed for MEDLINE]
239: Takemoto DJ, Dunford C, McMurray MM.
The cytotoxic and cytostatic effects of the bitter melon (Momordica charantia) on human lymphocytes.
Toxicon. 1982;20(3):593-9.
PMID: 7201686 [PubMed - indexed for MEDLINE]
240: Welihinda J, Arvidson G, Gylfe E, Hellman B, Karlsson E.
The insulin-releasing activity of the tropical plant momordica charantia.
Acta Biol Med Ger. 1982;41(12):1229-40.
PMID: 6765165 [PubMed - indexed for MEDLINE]
241: Foa-Tomasi L, Campadelli-Fiume G, Barbieri L, Stirpe F.
Effect of ribosome-inactivating proteins on virus-infected cells. Inhibition of virus multiplication and of protein synthesis.
Arch Virol. 1982;71(4):323-32.
PMID: 6284092 [PubMed - indexed for MEDLINE]
242: Takemoto DJ, Jilka C, Kresie R.
Purification and characterization of a cytostatic factor from the bitter melon Momordica charantia.
Prep Biochem. 1982;12(4):355-75.
PMID: 6185939 [PubMed - indexed for MEDLINE]
243: Takemoto DJ, Dunford C, Vaughn D, Kramer KJ, Smith A, Powell RG.
Guanylate cyclase activity in human leukemic and normal lymphocytes. Enzyme inhibition and cytotoxicity of plant extracts.
Enzyme. 1982;27(3):179-88.
PMID: 6122565 [PubMed - indexed for MEDLINE]
244: Khanna P, Jain SC, Panagariya A, Dixit VP.
Hypoglycemic activity of polypeptide-p from a plant source.
J Nat Prod. 1981 Nov-Dec;44(6):648-55.
PMID: 7334382 [PubMed - indexed for MEDLINE]
245: Akhtar MS, Athar MA, Yaqub M.
Effect of Momordica charantia on blood glucose level of normal and alloxan-diabetic rabbits.
Planta Med. 1981 Jul;42(3):205-12. No abstract available.
PMID: 7280086 [PubMed - indexed for MEDLINE]
246: Leatherdale BA, Panesar RK, Singh G, Atkins TW, Bailey CJ, Bignell AH.
Improvement in glucose tolerance due to Momordica charantia (karela).
Br Med J (Clin Res Ed). 1981 Jun 6;282(6279):1823-4.
PMID: 6786635 [PubMed - indexed for MEDLINE]
247: Das MK, Khan MI, Surolia A.
Fluorimetric studies of the binding of Momordica charantia (bitter gourd) lectin with ligands.
Biochem J. 1981 Apr 1;195(1):341-3.
PMID: 7306061 [PubMed - indexed for MEDLINE]
248: Khan MI, Mazumder T, Pain D, Gaur N, Surolia A.
Binding of 4-methylumbelliferyl beta-D-galactopyranoside to Momordica charantia lectin:
fluorescence-quenching studies.
Eur J Biochem. 1981 Jan;113(3):471-6.
PMID: 7215338 [PubMed - indexed for MEDLINE]
249: Mazumder T, Gaur N, Surolia A.
The physicochemical properties of the galactose-specific lectin from Momordica charantia.
Eur J Biochem. 1981 Jan;113(3):463-70.
PMID: 7215337 [PubMed - indexed for MEDLINE]
250: Horejsi V, Ticha M, Novotny J, Kocourek J.
Studies on lectins. XLVII. Some properties of D-galactose binding lectins isolated from the seeds of Butea frondosa, Erythrina indica and Momordica charantia.
Biochim Biophys Acta. 1980 Jun 26;623(2):439-48.
PMID: 7397226 [PubMed - indexed for MEDLINE]
251: Li SS.
Purification and partial characterization of two lectins from Momordica charantia.
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Crystallization and preliminary X-ray diffraction analysis of a plant ribonuclease from the seeds of the bitter gourd Momordica charantia.
J Mol Biol. 1992 Dec 20;228(4):1271-3.
PMID: 1474592 [PubMed - indexed for MEDLINE]
179: Higashino H, Suzuki A, Tanaka Y, Pootakham K.
[Hypoglycemic effects of Siamese Momordica charantia and Phyllanthus urinaria extracts in streptozotocin-induced diabetic rats (the lst report)]
Nippon Yakurigaku Zasshi. 1992 Nov;100(5):415-21. Japanese.
PMID: 1464400 [PubMed - indexed for MEDLINE]
180: Battelli MG, Montacuti V, Stirpe F.
High sensitivity of cultured human trophoblasts to ribosome-inactivating proteins.
Exp Cell Res. 1992 Jul;201(1):109-12.
PMID: 1612115 [PubMed - indexed for MEDLINE]
181: Ng TB, Chan WY, YeungHW.
Proteins with abortifacient, ribosome inactivating, immunomodulatory, antitumor and anti-AIDS activities from Cucurbitaceae plants.
Gen Pharmacol. 1992 Jul;23(4):579-90. Review.
PMID: 1397965 [PubMed - indexed for MEDLINE]
182: Huang Q, Liu S, Tang Y, Zeng F, Qian R.
Amino acid sequencing of a trypsin inhibitor by refined 1.6 A X-ray crystal structure of its complex with porcine beta-trypsin.
FEBS Lett. 1992 Feb 3;297(1-2):143-6.
PMID: 1551419 [PubMed - indexed for MEDLINE]
183: Omi T, Kamesaki T, Kajii E, Ikemoto S.
Method for detecting the lectin activity of Momordica charantia transferred from micro two-dimensional electrophoretic gel on to nitrocellulose.
J Chromatogr. 1991 Oct 4;570(2):399-405.
PMID: 1797856 [PubMed - indexed for MEDLINE]
184: Ogata F, Miyata T, Fuiii N, Yoshida N, Noda K, Makisumi S, Ito A.
Purification and amino acid sequence of a bitter gourd inhibitor against an acidic amino acid-specific endopeptidase of Streptomyces griseus.
J Biol Chem. 1991 Sep 5;266(25):16715-21.
PMID: 1679433 [PubMed - indexed for MEDLINE]
185: Ide H, Kimura M, Arai M, Funatsu G.
The complete amino acid sequence of ribonuclease from the seeds of bitter gourd (Momordica charantia).
FEBS Lett. 1991 Sep 2;289(l):126. No abstract available.
PMID: 1894001 [PubMed - indexed for MEDLINE]
186: Giron LM, Freire V, Alonzo A, Caceres A.
Ethnobotanical survey of the medicinal flora used by the Caribs of Guatemala.
J Ethnopharmacol. 1991 Sep;34(2-3):173-87.
PMID: 1795521 [PubMed - indexed for MEDLINE]
187: Kimura Y, Minami Y, Tokuda T, Nakajima S, Takagi S, Funatsu G.
Primary structures of N-linked oligosaccharides of momordin-a, a ribosome-inactivating protein from Momordica charantia seeds.
Agric Biol Chem. 1991 Aug;55(8):2031-6.
PMID: 1368729 [PubMed - indexed for MEDLINE]
188: Zafar R, Neerj a.
Momordica charantia--a review.
Hamdard Med. 1991 Jul-Sep;34(3):49-61. No abstract available.
PMID: 11613982 [PubMed - indexed for MEDLINE]
189: Yeung HW, Li WW, Ng TB.
Isolation of a ribosome-inactivating and abortifacient protein from seeds of Luffa acutangula.
Int J Pept Protein Res. 1991 Ju1;38(1):15-9.
PMID: 1938101 [PubMed - indexed for MEDLINE]
190: Ide H, Kimura M, Arai M, Funatsu G.
The complete amino acid sequence of ribonuclease from the seeds of bitter gourd (Momordica charantia).
FEBS Lett. 1991 Jun 24;284(2):161-4. Erratum in: FEBS Lett. 1991 Sep 2;289(1):126.
PMID: 2060635 [PubMed - indexed for MEDLINE]
191: Ho WK, Liu SC, Shaw PC, Yeung HW, Ng TB, Chan WY.
Cloning of the cDNA of alpha-momorcharin: a ribosome inactivating protein.
Biochim Biophys Acta. 1991 Feb 16;1088(2):311-4.
PMID: 2001404 [PubMed - indexed for MEDLINE]
192: Biswas AR, Ramaswamy S, Bapna JS.
Analgesic effect of Momordica charantia seed extract in mice and rats.
J Ethnopharmacol. 1991 Jan;31(1):115-8. No abstract available.
PMID: 2030591 [PubMed - indexed for MEDLINE]
193: Amorim CZ, Marques AD, Cordeiro RS.
Screening of the antimalarial activity of plants of the Cucurbitaceae family.
Mem Inst Oswaldo Cruz. 1991;86 Supp12:177-80.
PMID: 1841996 [PubMed - indexed for MEDLINE]
194: Lee-Huang S, Huang PL, Nara PL, Chen HC, Kung HF, HuangP, Huaniz HI, Huang PL.
MAP 30: a new inhibitor of HIV-1 infection and replication.
FEBS Lett. 1990 Oct 15;272(1-2):12-8.
PMID: 1699801 [PubMed - indexed for MEDLINE]
195: Day C, Cartwright T, Provost J, BaileY CJ.
Hypoglycaemic effect of Momordica charantia extracts.
Planta Med. 1990 Oct;56(5):426-9.
PMID: 2077547 [PubMed - indexed for MEDLINE]
196: Karunanayake EH, Jeevathayaparan S, Tennekoon KH.
Effect of Momordica charantia fruit juice on streptozotocin-induced diabetes in rats.
J Ethnopharmacol. 1990 Sep;30(2):199-204.
PMID: 2255210 [PubMed - indexed for MEDLINE]
197: Guevara AP, Lim-Sylianco C, Dayrit F, Finch P.
Antimutagens from Momordica charantia.
Mutat Res. 1990 Jun;230(2):121-6.
PMID: 2115617 [PubMed - indexed for MEDLINE]
198: Cunnick JE, Sakamoto K, Chapes SK, Fortner GW, Takemoto DJ.
Induction of tumor cytotoxic immune cells using a protein from the bitter melon (Momordica charantia).
Cell Immunol. 1990 Apr 1;126(2):278-89.
PMID: 2311123 [PubMed - indexed for MEDLINE]
199: Kamesaki T, Omi T, Kajii E, Ikemoto S.
New method of detecting the lectin activity of Momordica charantia.
Vox Sang. 1990;58(4):307-8. No abstract available.
PMID: 2399697 [PubMed - indexed for MEDLINE]
200: Zhu ZJ, Zhong ZC, Luo ZY, Xiao ZY.
[Studies on the active constituents of Momordica charantia L]
Yao Xue Xue Bao. 1990;25(12):898-903. Chinese.
PMID: 2104468 [PubMed - indexed for MEDLINE]
201: Chandrasekar B, Mukherjee B, Mukheriee SK.
Blood sugar lowering potentiality of selected Cucurbitaceae plants of Indian origin.
Indian J Med Res. 1989 Aug;90:300-5.
PMID: 2620957 [PubMed - indexed for MEDLINE]
202: Singh N, Tyagi SD, Agarwal SC.
Effects of long term feeding of acetone extract of Momordica charantia (whole fruit powder) on alloxan diabetic albino rats.
Indian J Physiol Pharmacol. 1989 Apr-Jun;33(2):97-100.
PMID: 2777367 [PubMed - indexed for MEDLINE]
203: Montecucchi PC, Lazzarini AM, Barbieri L, Stir_pe F, Soria M, Lappi D.
N-terminal sequence of some ribosome-inactivating proteins.
Int J Pept Protein Res. 1989 Apr;33(4):263-7.
PMID: 2753596 [PubMed - indexed for MEDLINE]
204: Hara S, Makino J, Ikenaka T.
Amino acid sequences and disulfide bridges of serine proteinase inhibitors from bitter gourd (Momordica charantia LINN.) seeds.
J Biochem (Tokyo). 1989 Jan;105(l):88-91.
PMID: 2738047 [PubMed - indexed for MEDLINE]
205: Ng TB, Li WW, Yeung HW.
Effects of lectins with various carbohydrate binding specificities on lipid metabolisni in isolated rat and hamster adipocytes.
Int J Biochem. 1989;21(2):149-55.
PMID: 2545472 [PubMed - indexed for MEDLINE]
206: Stirpe F, Wawrzynczak EJ, Brown AN, Knyba RE, Watson GJ, Barbieri L, Thorpe PE.
Selective cytotoxic activity of immunotoxins composed of a monoclonal anti-Thy 1.1 antibody and the ribosome-inactivating proteins bryodin and momordin.
Br J Cancer. 1988 Nov;58(5):558-61.
PMID: 3265330 [PubMed - indexed for MEDLINE]
207: Srivastava Y, Venkatakrishna-Bhatt H, Verma Y.
Effect of Momordica charantia Linn. pomous aqueous extract on cataractogenesis in murrin alloxan diabetics.
Pharmacol Res Commun. 1988 Mar;20(3):201-9.
PMID: 3387455 [PubMed - indexed for MEDLINE]
208: Yeung HW, Li WW, Feng Z, Barbieri L, Stirpe F.
Trichosanthin, alpha-momorcharin and beta-momorcharin: identity of abortifacient and ribosome-inactivating proteins.
Int J Pept Protein Res. 1988 Mar;31(3):265-8.
PMID: 3372132 [PubMed - indexed for MEDLINE]
209: Ng TB, Tam PP, Hon WK, Choi HL, Yeung HW.
Effects of momorcharins on ovarian response to gonadotropin-induced superovulation in mice.
Int J Fertil. 1988 Mar-Apr;33(2):123-8.
PMID: 2898450 [PubMed - indexed for MEDLINE]
210: Ng TB, Li WW, Yeung HW.
Effects of ginsenosides, lectins and Momordica charantia insulin-like peptide on corticosterone production by isolated rat adrenal cells.
J Ethnopharmacol. 1987 Sep-Oct;21(1):21-9.
PMID: 2826928 [PubMed - indexed for MEDLINE]
211: Srivastava Y, Venkatakrishna-Bhatt H, Verma Y, Prem AS.
Retardation of retinopathy by Momordica charantia L. (bitter gourd) fruit extract in alloxan diabetic rats.
Indian J Exp Biol. 1987 Aug;25(8):571-2. No abstract available.
PMID: 3446597 [PubMed - indexed for MEDLINE]
212: Leung SO, Yeung HW, Leung KN.
The immunosuppressive activities of two abortifacient proteins isolated from the seeds of bitter melon (Momordica charantia).
Immunopharmacology. 1987 Jun;13(3):159-71.
PMLD: 3497134 [PubMed - indexed for MEDLINE]
213: Ng TB, Wong CM, Li WW, Yeung HW.
Acid-ethanol extractable compounds from fruits and seeds of the bitter gourd Momordica charantia: effects on lipid metabolism in isolated rat adipocytes.
Am J Chin Med. 1987;15(1-2):31-42.
PMID: 3318384 [PubMed - indexed for MEDLINE]
214: Ng TB, Wong CM, Li WW, Yeung HW.
Peptides with antilipolytic and lipogenic activities from seeds of the bitter gourd Momordica charantia (family Cucurbitaceae).
Gen Pharmacol. 1987;18(3):275-81.
PMID: 3106137 [PubMed - indexed for MEDLINE]
215: Chan WY, Tam PP, Choi HL, Ng TB, Yeung HW.
Effects of momorcharins on the mouse embryo at the early organogenesis stage.
Contraception. 1986 Nov;34(5):537-44.
PMID: 3816236 [PubMed - indexed for MEDLINE]
216: Welihinda J, Karunanayake EH, Sheriff MH, Jayasinghe KS.
Effect of Momordica charantia on the glucose tolerance in maturity onset diabetes.
J Ethnopharmacol. 1986 Sep;17(3):277-82.
PMID: 3807390 [PubMed - indexed for MEDLINE]
217: Welihinda J, Karunanayake EH. , Extra-pancreatic effects of Momordica charantia in rats.
J Ethnopharmacol. 1986 Sep;17(3):247-55.
PMID: 3807387 [PubMed - indexed for MEDLINE]
218: Ng TB, Wong CM, Li WW, Yeung HW.
Isolation and characterization of a galactose binding lectin with insulinomimetic activities.
From the seeds of the bitter gourd Momordica charantia (Family Cucurbitaceae).
Int J Pept Protein Res. 1986 Aug;28(2):163-72.
PMID: 3533814 [PubMed - indexed for MEDLINE]
219: Ng TB, Wong CM, Li WW, Yeung HW.
A steryl glycoside fraction from Momordica charantia seeds with an inhibitory action on lipid metabolism in vitro.
Biochem Cell Biol. 1986 Aug;64(8):766-71.
PMID: 3021185 [PubMed - indexed for MEDLINE]
220: Ng TB, Wong CM, Li WW, Yeung HW.
Insulin-like molecules in Momordica charantia seeds.
J Ethnopharmacol. 1986 Jan;15(1):107-17.
PMID: 3520153 [PubMed - indexed for MEDLINE]
221: Wong CM, Yeung HW, Ng TB.
Screening of Trichosanthes kirilowii, Momordica charantia and Cucurbita maxima (family Cucurbitaceae) for compounds with antilipolytic activity.
J Ethnopharmacol. 1985 Jul;13(3):313-21.
PMID: 4058034 [PubMed - indexed for MEDLINE]
222: Lappi DA, Esch FS, Barbieri L, Stirpe F, Soria M.
Characterization of a Saponaria officinalis seed ribosome-inactivating protein:
immunoreactivity and sequence homologies.
Biochem Biophys Res Commun. 1985 Jun 28;129(3):934-42.
PMID: 3925952 [PubMed - indexed for MEDLINE]
223: Lei QJ, Jiang XM, Luo AC, Liu ZF, He XC, Wang XD, Cui FY, Chen PX.
Influence of balsam pear (the fruit of Momordica charantia L.) on blood sugar level.
J Tradit Chin Med. 1985 Jun;5(2):99-106. No abstract available.
PMID: 3851122 [PubMed - indexed for MEDLINE]
224: Bailey CJ, Day C, Turner SL, Leatherdale BA.
Cerasee, a traditional treatment for diabetes. Studies in normal and streptozotocin diabetic mice.
Diabetes Res. 1985 Mar;2(2):81-4.
PMID: 3899464 [PubMed - indexed for MEDLINE]
225: Meir P, Yaniv Z.
An in vitro study on the effect of Momordica charantia on glucose uptake and glucose metabolism in rats.
Planta Med. 1985 Feb;(1):12-6. No abstract available.
PMID: 4011748 [PubMed - indexed for MEDLINE]
226: Chan WY, Tam PP, So KC, Yeung HW.
The inhibitory effects of beta-momorcharin on endometrial cells in the mouse.
Contraception. 1985 Jan;31(1):83-90.
PMID: 3987275 [PubMed - indexed for MEDLINE]
227: Karunanayake EH, Welihinda J, Sirimanne SR, Sinnadorai G.
Oral hypoglycaemic activity of some medicinal plants of Sri Lanka.
J Etlinopharmacol. 1984 Jul;11(2):223-31.
PMID: 6492834 [PubMed - indexed for MEDLINE]
228: Foxwell B, Long J, Stiipe F.
Cytoxicity of erythrocyte ghosts loaded with ribosome-inactivating proteins following fusion with CHO cells.
Biochem Int. 1984 Jun;8(6):811-9.
PMID: 6541045 [PubMed - indexed for MEDLINE]
229: Chan WY, Tam PP, Yeung HW.
The termination of early pregnancy in the mouse by beta-momorcharin.
Contraception. 1984 Jan;29(1):91-100.
PMID: 6734206 [PubMed - indexed for MEDLINE]
230: Jilka C, Strifler B, Fortner GW, Hays EF, Takemoto DJ.
In vivo antitumor activity of the bitter melon (Momordica charantia).
Cancer Res. 1983 Nov;43(11):5151-5.
PMID: 6616452 [PubMed - indexed for MEDLINE]
231: Sargiacomo M, Barbieri L, Stirpe F, Tomasi M.
Cytotoxicity acquired by ribosome-inactivating proteins carried by reconstituted Sendai virus envelopes.
FEBS Lett. 1983 Jun 27;157(1):150-4.
PMID: 6305714 [PubMed - indexed for MEDLINE]
232: Spreafico F, Malfiore C, Moras ML, Marmonti L, Filippeschi S, Barbieri L, Perocco P, Stirpe F.
The immunomodulatory activity of the plant proteins Momordica charantia inhibitor and pokeweed antiviral protein.
Int J Immunopharmacol. 1983;5(4):335-43.
PMID: 6629594 [PubMed - indexed for MEDLINE]
233: Takemoto DJ, Jilka C, Rockenbach S, Hu heg s JV.
Purification and characterization of a cytostatic factor with anti-viral activity from the bitter melon.
Prep Biochem. 1983;13(4):371-93.
PMID: 6196772 [PubMed - indexed for MEDLINE]
234: Takemoto DJ, Jilka C, Rockenbach S, Hughes JV.
Purification and characterization of a cytostatic factor with anti-viral activity from the bitter melon.
Prep Biochem. 1983;13(5):397-421.
PMID: 6142453 [PubMed - indexed for MEDLINE]
235: Falasca A, Gasperi-Campani A, Abbondanza A, Barbieri L, Stirpe F.
Properties of the ribosome-inactivating proteins gelonin, Momordica charantia inhibitor, and dianthins.
Biochem J. 1982 Dec 1;207(3):505-9.
PMID: 6819861 [PubMed - indexed for MEDLINE]
236: Farnsworth NR, Waller DP.
Current status of plant products reported to inhibit sperm.
Res Front Fertil Regul. 1982 Jun;2(1):1-16.
PMID: 12179631 [PubMed - indexed for MEDLINE]
237: Akhtar MS.
Trial of Momordica charantia Linn (Karela) powder in patients with maturity-onset diabetes.
J Pak Med Assoc. 1982 Apr;32(4):106-7. No abstract available.
PMID: 6806502 [PubMed - indexed for MEDLINE]
238: Kedar P, Chakrabarti CH.
Effects of bittergourd (Momordica charantia) seed & glibenclamide in streptozotocin induced diabetes mellitus.
Indian J Exp Biol. 1982 Mar;20(3):232-5. No abstract available.
PMID: 6811427 [PubMed - indexed for MEDLINE]
239: Takemoto DJ, Dunford C, McMurray MM.
The cytotoxic and cytostatic effects of the bitter melon (Momordica charantia) on human lymphocytes.
Toxicon. 1982;20(3):593-9.
PMID: 7201686 [PubMed - indexed for MEDLINE]
240: Welihinda J, Arvidson G, Gylfe E, Hellman B, Karlsson E.
The insulin-releasing activity of the tropical plant momordica charantia.
Acta Biol Med Ger. 1982;41(12):1229-40.
PMID: 6765165 [PubMed - indexed for MEDLINE]
241: Foa-Tomasi L, Campadelli-Fiume G, Barbieri L, Stirpe F.
Effect of ribosome-inactivating proteins on virus-infected cells. Inhibition of virus multiplication and of protein synthesis.
Arch Virol. 1982;71(4):323-32.
PMID: 6284092 [PubMed - indexed for MEDLINE]
242: Takemoto DJ, Jilka C, Kresie R.
Purification and characterization of a cytostatic factor from the bitter melon Momordica charantia.
Prep Biochem. 1982;12(4):355-75.
PMID: 6185939 [PubMed - indexed for MEDLINE]
243: Takemoto DJ, Dunford C, Vaughn D, Kramer KJ, Smith A, Powell RG.
Guanylate cyclase activity in human leukemic and normal lymphocytes. Enzyme inhibition and cytotoxicity of plant extracts.
Enzyme. 1982;27(3):179-88.
PMID: 6122565 [PubMed - indexed for MEDLINE]
244: Khanna P, Jain SC, Panagariya A, Dixit VP.
Hypoglycemic activity of polypeptide-p from a plant source.
J Nat Prod. 1981 Nov-Dec;44(6):648-55.
PMID: 7334382 [PubMed - indexed for MEDLINE]
245: Akhtar MS, Athar MA, Yaqub M.
Effect of Momordica charantia on blood glucose level of normal and alloxan-diabetic rabbits.
Planta Med. 1981 Jul;42(3):205-12. No abstract available.
PMID: 7280086 [PubMed - indexed for MEDLINE]
246: Leatherdale BA, Panesar RK, Singh G, Atkins TW, Bailey CJ, Bignell AH.
Improvement in glucose tolerance due to Momordica charantia (karela).
Br Med J (Clin Res Ed). 1981 Jun 6;282(6279):1823-4.
PMID: 6786635 [PubMed - indexed for MEDLINE]
247: Das MK, Khan MI, Surolia A.
Fluorimetric studies of the binding of Momordica charantia (bitter gourd) lectin with ligands.
Biochem J. 1981 Apr 1;195(1):341-3.
PMID: 7306061 [PubMed - indexed for MEDLINE]
248: Khan MI, Mazumder T, Pain D, Gaur N, Surolia A.
Binding of 4-methylumbelliferyl beta-D-galactopyranoside to Momordica charantia lectin:
fluorescence-quenching studies.
Eur J Biochem. 1981 Jan;113(3):471-6.
PMID: 7215338 [PubMed - indexed for MEDLINE]
249: Mazumder T, Gaur N, Surolia A.
The physicochemical properties of the galactose-specific lectin from Momordica charantia.
Eur J Biochem. 1981 Jan;113(3):463-70.
PMID: 7215337 [PubMed - indexed for MEDLINE]
250: Horejsi V, Ticha M, Novotny J, Kocourek J.
Studies on lectins. XLVII. Some properties of D-galactose binding lectins isolated from the seeds of Butea frondosa, Erythrina indica and Momordica charantia.
Biochim Biophys Acta. 1980 Jun 26;623(2):439-48.
PMID: 7397226 [PubMed - indexed for MEDLINE]
251: Li SS.
Purification and partial characterization of two lectins from Momordica charantia.
Experientia. 1980 May 15;36(5):524-7.
PMID: 7379938 [PubMed - indexed for MEDLINE]
252: Takemoto DJ, Kresie R, Vaughn D.
Partial purification and characterization of a guanylate cyclase inhibitor with cytotoxic properties from the bitter melon (Momordica charantia).
Biochem Biophys Res Commun. 1980 May 14;94(1):332-9. No abstract available.
PMID: 6104489 [PubMed - indexed for MEDLINE]
253: Barbieri L, Zamboni M, Lorenzoni E, Montanaro L, Sperti S, Stirpe F.
Inhibition of protein synthesis in vitro by proteins from the seeds of Momordica charantia (bitter pear melon).
Biochem J. 1980 Feb 15;186(2):443-52.
PMID: 7378061 [PubMed - indexed for MEDLINE]
254: Licastro F, Franceschi C, Barbieri L, Stir2e F.
Toxicity of Momordica charantia lectin and inhibitor for human normal and leukaemic lymphocytes.
Virchows Arch B Cell Pathol Incl Mol Pathol. 1980;33(3):257-65.
PMID: 6110273 [PubMed - indexed for MEDLINE]
255: Barbieri L, Lorenzoni E, Stirpe F.
Inhibition of protein synthesis in vitro by a lectin from Momordica charantia and by other haemagglutinins.
Biochem J. 1979 Aug 15;182(2):633-5.
PMID: 508306 [PubMed - indexed for MEDLINE]
256: Dixit VP, Khanna P, Bhargava SK.
Effects of Momordica charantia L. fruit extract on the testicular function of dog.
Planta Med. 1978 Nov;34(3):280-6. No abstract available.
PMTD: 704696 [PubMed - indexed for MEDLINE]
257: Claflin AJ, Vesely DL, Hudson JL, Bagwell CB, Lehotay DC, Lo TM, Fletcher MA, Block NL, Levey GS.
Inhibition of growth and guanylate cyclase activity of an undifferentiated prostate adenocarcinoma by an extract of the balsam pear (Momordica charantia abbreviata).
Proc Natl Acad Sci U S A. 1978 Feb;75(2):989-93.
PMID: 24847 [PubMed - indexed for MEDLINE]
258: Lin JY, Hou MJ, Chen YC.
Isolation of toxic and non-toxic lectins from the bitter pear melon Momordica charantia Linn.
Toxicon. 1978;16(6):653-60. No abstract available.
PMID: 725959 [PubMed - indexed for MEDLINE]
259: Vesely DL, Graves WR, Lo TM, Fletcher MA, Levey GS.
Isolation of a guanylate cyclase inhibitor from the balsam pear (Momordica charantia abreviata).
Biochem Biophys Res Commun. 1977 Aug 22;77(4):1294-9. No abstract available.
PMID: 20099 [PubMed - indexed for MEDLINE]
260: Li SS.
Purification and characterization of seed storage proteins from Momordica charantia.
Experientia. 1977 Jul 15;33(7):895-6. No abstract available.
PMID: 891765 [PubMed - indexed for MEDLINE]
261: Foley RH.
Acute poisoning in a puppy caused by the balsam pear (Momordica charantia).
Vet Med Small Anim Clin. 1976 Jun;71(6):761-2. No abstract available.
PMID: 1047586 [PubMed - indexed for MEDLINE]
262: Lal J, Chandra S, Raviprakash V, Sabir M.
In vitro anthelmintic action of some indigenous medicinal plants on Ascardia galli worms.
Indian J Physiol Pharmacol. 1976 Apr-Jun;20(2):64-8.
PMID: 965077 [PubMed - indexed for MEDLINE]
263: West ME, Sidrak GH, Street SP.
The anti-growth properties of extracts from Momordica charantia L.
West Indian Med J. 1971 Mar;20(1):25-34. No abstract available.
PMID: 5104841 [PubMed - indexed for MEDLINE]
264: CHATTERJEE KP.
ON THE PRESENCE OF AN ANTIDIABETIC PRINCIPLE IN MOMORDICA
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Indian J Physiol Pharmacol. 1963 Oct;52:240-4. No abstract available.
PMID: 14175615 [PubMed - OLDMEDLINE for Pre] 966]
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15. Valero M, Salmeron MC. Antibacterial activity of 11 essential oils against Bacillus cereus in tyndallized carrot broth. IntJFood Microbiol. Aug 15;85(1-2):73-81.
16. VanderEnde DS, Morrow JD. Release of markedly increased quantities of prostaglandin D2 from the skin in vivo in humans after the application of cinnamic aldehyde. J Am Acad Dermato12001 Jul;45(1):62-7. Wood, Rebecca.
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18. Vanschoonbeek K, Thomassen BJ, Senden JM, Wodzig WK, van Loon LJ.
Cinnamon supplementation does not improve glycemic control in postmenopausal type 2 diabetes patients.J Nutr. 2006 Apr;136(4):977-80. PMID: 16549460 PubMed - in process]
19. Bousquet PJ, Guillot B, Guilhou JJ, Raison-Peyron N. A stomatitis due to artificial cinnamon-flavored chewing gum.Arch Dermatol. 2005 Nov;141(11):1466-7. No abstract available. PMID: 16301399 [PubMed - indexed for MEDLINE]
20. Schoene NW, Kelly MA, Polansky MM, Anderson RA.Water-soluble polymeric polyphenols from cinnamon inhibit proliferation and alter cell cycle distribution patterns of hematologic tumor cell lines.Cancer Lett. 2005 Dec 8;230(1):134-40.
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30. Friedman M, Buick R, Elliott CT.
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31. Lai PK, Roy J.
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32. Qin B, Nagasaki M, Ren M, Bajotto G, Oshida Y, Sato Y.
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polymers from cinnamon with insulin-like biological activity.J Agric Food Chem.
2004 Jan 14;52(1):65-70.
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34. Anderson RA, Broadhurst CL, Polansky MM, Schmidt WF, Khan A, Flanagan VP, Schoene NW, Graves DJ. Isolation and characterization of olyphenol type-A
polymers from cinnamon with insulin-like biological activity.J Agric Food Chem.
2004 Jan 14;52(1):65-70. PMID: 14709014 [PubMed - indexed for MEDLINE]
35. Anderson RA, Broadhurst CL, Polansky MM, Schmidt WF, Khan A, Flanagan VP, Schoene NW, Graves DJ. Isolation and characterization of olyphenol type-A
polymers from cinnamon with insulin-like biological activity.J Agric Food Chem.
2004 Jan 14;52(1):65-70. PMID: 14709014 [PubMed - indexed for MEDLINE]
36. Lee JS, Jeon SM, Park EM, Huh TL, Kwon OS, Lee MK, Choi MS.
Cinnamate supplementation enhances hepatic lipid metabolism and antioxidant defense systems in high cholesterol-fed rats.
J Med Food. 2003 Fall;6(3):183-91. PMID: 14585184 [PubMed - indexed for MEDLINE]
37. Qidwai W, Alim SR, Dhanani RH, Jehangir S, Nasrullah A, Raza A.
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39. Jayaprakasha GK, Jagan Mohan Rao L, Sakariah KKVolatile constituents from Cinnamomum zeylanicum fruit stalks and their antioxidant activities.
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50. Vanschoonbeek K, Thomassen BJW, Senden JM, Wodzig WKWH, Van Loon LJC. Cinnamon supplementation does not improve glycemic control in postmenopausal type 2 diabetes patients. J Nutr 2006; 136(4): 977-80.
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19(3): 203-6.
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Claims (54)
1. A new therapeutic formulation which comprises cinnamon and bitter melon.
2. A new therapeutic formulation which comprises cinnamon and bitter melon in a ratio of between 70:30 to 60:40.
3. A new therapeutic formulation which comprises cinnamon and bitter melon in a ratio of 70:30.
4. A new therapeutic formulation which comprises cinnamon and bitter melon in a ratio of 60:40.
5. A capsule containing 120 milligrams of bitter melon and 280 milligrams of cinnamon.
6. A capsule containing 150 milligrams of bitter melon and 250 milligrams of cinnamon.
7. A capsule containing 200 milligrams of bitter melon and 300 milligrams of cinnamon.
8. A new therapeutic formulation as claimed in claim 1 which comprises:
Cinnamon (Cinnamomi cassiae: Cinnamonum verum) 280 mg Bitter melon (Momordica charantia) 120 mg Diluent 151 mg Lubricant 3 mg
Cinnamon (Cinnamomi cassiae: Cinnamonum verum) 280 mg Bitter melon (Momordica charantia) 120 mg Diluent 151 mg Lubricant 3 mg
9. A new therapeutic formulation as claimed in claim 7 wherein the diluent is microcrystalline cellulose and dicalcium phosphate dihydrate.
10. A new therapeutic formulation as claimed in claim 8 wherein said microcrystalline cellulose is present in the amount of 150 milligrams and dicalcium phosphate dihydrate is present in the amount of one (1) milligram.
11. A new therapeutic formulation as claimed in claim 7 wherein the lubricant is magnesium stearate.
12. A compressed tablet containing 200 mg of bitter melon and 300 mg of cinnamon.
13. A new therapeutic formulation as claimed in claim 1 which is mixed in a chocolate vehicle.
14. A new therapeutic formulation as claimed in claim 2 which is mixed in a chocolate vehicle.
15. A new therapeutic formulation as claimed in claim 3 which is mixed in a chocolate vehicle.
16. A new therapeutic formulation as claimed in claim 4 which is mixed in a chocolate vehicle.
17. A new therapeutic formulation as claimed in claim 13 wherein said chocolate vehicle comprises a dark chocolate which comprises a mixture of forty-three percent (43%) maltitol, cocoa butter, cocoa powder processed with an alkali, a chocolate liquor, cocoa powder, milk fat, soya lecithin and natural flavours.
18. A new therapeutic formulation as claimed in claim 13 wherein said chocolate vehicle comprises a milk chocolate which contains maltitol in the amount of fifty-five percent (55%), cocoa butter, a chocolate liquor, calcium carbonate, milk fat, calcium caseinate, soya lecithin and vanilla extract.
19. A new therapeutic formulation as claimed in claim 13 wherein said chocolate vehicle comprises a high protein sucrose free milk chocolate which includes maltitol, fractionated modified palm kernel oil, milk protein concentrate, cocoa powder, calcium caseinate, soya lecithin and vanilla extract.
20. A new therapeutic formulation as claimed in claim 13 wherein said chocolate vehicle comprises a dark sugar free coating which is comprised of a chocolate liquor processed with an alkali, maltitol, cocoa butter, butter oil, soya lecithin and vanilla extract.
21. A new therapeutic formulation as claimed in claim 14 wherein said chocolate vehicle comprises a dark chocolate which comprises a mixture of forty-three percent (43%) maltitol, cocoa butter, cocoa powder processed with an alkali, a chocolate liquor, cocoa powder, milk fat, soya lecithin and natural flavours.
22. A new therapeutic formulation as claimed in claim 14 wherein said chocolate vehicle comprises a milk chocolate which contains maltitol in the amount of fifty-five percent (55%), cocoa butter, a chocolate liquor, calcium carbonate, milk fat, calcium caseinate, soya lecithin and vanilla extract.
23. A new therapeutic formulation as claimed in claim 14 wherein said chocolate vehicle comprises a high protein sucrose free milk chocolate which includes maltitol, fractionated modified palm kernel oil, milk protein concentrate, cocoa powder, calcium caseinate, soya lecithin and vanilla extract.
24. A new therapeutic formulation as claimed in claim 14 wherein said chocolate vehicle comprises a dark sugar free coating which is comprised of a chocolate liquor processed with an alkali, maltitol, cocoa butter, butter oil, soya lecithin and vanilla extract.
25. A new therapeutic formulation as claimed in claim 15 wherein said chocolate vehicle comprises a dark chocolate which comprises a mixture of forty-three percent (43%) maltitol, cocoa butter, cocoa powder processed with an alkali, a chocolate liquor, cocoa powder, milk fat, soya lecithin and natural flavours.
26. A new therapeutic formulation as claimed in claim 15 wherein said chocolate vehicle comprises a milk chocolate which contains maltitol in the amount of fifty-five percent (55%), cocoa butter, a chocolate liquor, calcium carbonate, milk fat, calcium caseinate, soya lecithin and vanilla extract.
27. A new therapeutic formulation as claimed in claim 15 wherein said chocolate vehicle comprises a high protein sucrose free milk chocolate which includes maltitol, fractionated modified palm kernel oil, milk protein concentrate, cocoa powder, calcium caseinate, soya lecithin and vanilla extract.
28. A new therapeutic formulation as claimed in claim 15 wherein said chocolate vehicle comprises a dark sugar free coating which is comprised of a chocolate liquor processed with an alkali, maltitol, cocoa butter, butter oil, soya lecithin and vanilla extract.
29. A new therapeutic formulation as claimed in claim 16 wherein said chocolate vehicle comprises a dark chocolate which comprises a mixture of forty-three percent (43%) maltitol, cocoa butter, cocoa powder processed with an alkali, a chocolate liquor, cocoa powder, milk fat, soya lecithin and natural flavours.
30. A new therapeutic formulation as claimed in claim 16 wherein said chocolate vehicle comprises a milk chocolate which contains maltitol in the amount of fifty-five percent (55%), cocoa butter, a chocolate liquor, calcium carbonate, milk fat, calcium caseinate, soya lecithin and vanilla extract.
31. A new therapeutic formulation as claimed in claim 16 wherein said chocolate vehicle comprises a high protein sucrose free milk chocolate which includes maltitol, fractionated modified palm kernel oil, milk protein concentrate, cocoa powder, calcium caseinate, soya lecithin and vanilla extract.
32. A new therapeutic formulation as claimed in claim 16 wherein said chocolate vehicle comprises a dark sugar free coating which is comprised of a chocolate liquor processed with an alkali, maltitol, cocoa butter, butter oil, soya lecithin and vanilla extract.
33. A novel therapeutic formulation as claimed in claim 1 further including omega-3 fatty acids.
34. A novel therapeutic formulation as claimed in claim 13 further including omega-3 fatty acids.
35. A novel therapeutic formulation as claimed in claim 14 further including omega-3 fatty acids.
36. A novel therapeutic formulation as claimed in claim 15 further including omega-3 fatty acids.
37. A novel therapeutic formulation as claimed in claim 16 further including omega-3 fatty acids.
38. A novel therapeutic formulation as claimed in claim 17 further including omega-3 fatty acids.
39. A novel therapeutic formulation as claimed in claim 18 further including omega-3 fatty acids.
40. A novel therapeutic formulation as claimed in claim 19 further including omega-3 fatty acids.
41. A novel therapeutic formulation as claimed in claim 20 further including omega-3 fatty acids.
42. A novel therapeutic formulation as claimed in claim 21 further including omega-3 fatty acids.
43. A novel therapeutic formulation as claimed in claim 22 further including omega-3 fatty acids.
44. A novel therapeutic formulation as claimed in claim 23 further including omega-3 fatty acids.
45. A novel therapeutic formulation as claimed in claim 24 further including omega-3 fatty acids.
46. A novel therapeutic formulation as claimed in claim 25 further including omega-3 fatty acids.
47. A novel therapeutic formulation as claimed in claim 26 further including omega-3 fatty acids.
48. A novel therapeutic formulation as claimed in claim 27 further including omega-3 fatty acids.
49. A novel therapeutic formulation as claimed in claim 28 further including omega-3 fatty acids.
50. A novel therapeutic formulation as claimed in claim 29 further including omega-3 fatty acids.
51. A novel therapeutic formulation as claimed in claim 30 further including omega-3 fatty acids.
52. A novel therapeutic formulation as claimed in claim 31 further including omega-3 fatty acids.
53. A novel therapeutic formulation as claimed in claim 32 further including omega-3 fatty acids.
54. A novel therapeutic product as claimed in claim 1 which comprises cinnamon in an amount of between 150 mg to 1000 mg, bitter melon in the amount of between 100 mg to about 1000 mg and omega-3 powder in the amount of between about 100 mg to about 1000 mg per 40 grams of product.
Priority Applications (2)
Application Number | Priority Date | Filing Date | Title |
---|---|---|---|
CA002567621A CA2567621A1 (en) | 2006-11-10 | 2006-11-10 | Herbal product comprising cinnamon, bitter melon and omega-3 fatty acids |
PCT/CA2007/002060 WO2008055363A1 (en) | 2006-11-10 | 2007-11-13 | Herbal product comprising cinnamon, bitter melon and omega-3 fatty acids |
Applications Claiming Priority (1)
Application Number | Priority Date | Filing Date | Title |
---|---|---|---|
CA002567621A CA2567621A1 (en) | 2006-11-10 | 2006-11-10 | Herbal product comprising cinnamon, bitter melon and omega-3 fatty acids |
Publications (1)
Publication Number | Publication Date |
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CA2567621A1 true CA2567621A1 (en) | 2008-05-10 |
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ID=39364154
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CA002567621A Abandoned CA2567621A1 (en) | 2006-11-10 | 2006-11-10 | Herbal product comprising cinnamon, bitter melon and omega-3 fatty acids |
Country Status (2)
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CA (1) | CA2567621A1 (en) |
WO (1) | WO2008055363A1 (en) |
Families Citing this family (4)
Publication number | Priority date | Publication date | Assignee | Title |
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US9918489B2 (en) | 2008-12-17 | 2018-03-20 | Mark Gorris | Food-based supplement delivery system |
TWI643630B (en) * | 2018-01-10 | 2018-12-11 | 寰宇生物科技股份有限公司 | Use of bitter gourd seed oil for preparing antibody fat forming preparation |
CN113116880B (en) * | 2021-05-25 | 2022-11-11 | 西南大学 | Application of herpetospermum elegans extract in preparation of medicine for treating non-alcoholic fatty liver disease |
WO2024038335A1 (en) * | 2022-08-18 | 2024-02-22 | GUPTE, Vaidehi Korde | Nutraceutical formulations to tackle weight related ailments |
Family Cites Families (4)
Publication number | Priority date | Publication date | Assignee | Title |
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US7014872B2 (en) * | 2002-03-26 | 2006-03-21 | Council Of Scientific And Industrial Research | Herbal nutraceutical formulation for diabetics and process for preparing the same |
US6787163B2 (en) * | 2003-01-21 | 2004-09-07 | Dennis H. Harris | Therapeutic treatment for blood sugar regulation |
US20050118324A1 (en) * | 2003-12-02 | 2005-06-02 | Mathew Anna M. | Good living tea - a diabetic dietary supplement drink |
CA2551706A1 (en) * | 2006-06-27 | 2007-12-27 | Innovative Life Sciences Corporation | Herbal product comprising cinnamon and bitter melon |
-
2006
- 2006-11-10 CA CA002567621A patent/CA2567621A1/en not_active Abandoned
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2007
- 2007-11-13 WO PCT/CA2007/002060 patent/WO2008055363A1/en active Application Filing
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