KR20120055095A - Composition comprising the powdered salted shrimp, the polar solvent soluble extract or insoluble extract thereof for preventing and treating obesity or hyperlipidemia and atherosclerotic-vascular diseases - Google Patents

Abstract

PURPOSE: A composition containing salted-fermented shrimp extract is provided to reduce lipid content in liver tissue and feces. CONSTITUTION: A pharmaceutical composition for preventing and treating obesity, hyperlipidemia and artheriosclerotic vascular diseases contains salted-fermented shrimp powder or polar solvent soluble extract or polar solvent insoluble extract thereof as an active ingredient. The polar solvent soluble extract is prepared using water including purified water, low carbon number alcohol, or mixture solvent thereof. A health food for preventing and treating obesity or hyperlipidemia and arteriosclerotic vascular diseases contains salted-fermented shrimp powder or polar solvent soluble extract or polar solvent insoluble extract thereof as an active ingredient. The health food includes powder, granules, tablets, capsules, or beverage.

Description

Composition containing the powdered salted shrimp, the polar solvent soluble extract or insoluble extract forth for preventing and treating obesity or hyperlipidemia and atherosclerotic-vascular diseases}

The present invention relates to a composition for the prevention and treatment of obesity or hyperlipidemia and atherosclerotic vascular disease containing shrimp powder, shrimp soluble organic solvent soluble extract or insoluble residue as an active ingredient.

[Reference 1] Bae SW, Choi SY, Jin HS, Kim CW, Lee KE, Kang ES, Park JY, Hong SP, Choi HY, Jung JH, Kim YS and Hong CS. 2003. Changes of allergenecity of salted and fermented shrimp. J Asthma Allergy Clin Immunol 23, p 44-52.

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[4] Friedewald WT, Levy RF and Frederickson DS. 1972.Estimation of the concentration low density lipoprotein cholesterol in plasma, without use of preparative ultra-centrifuge. Clin . Chem 18, p 499-602.

Hayashi H, Shitara M and Yamasaki F. 1982. The origin of lipid accumulated in the liver lysosomes after administration of triton WR-1339. J. Biochem. 92, p 1585-1590.

Document 6 Hsu HC, Lee YT and Chen MF. 2000. Effect of n-3 fatty acids on the composition and binding properties of lipoproteins in hypertriglyceridemic patients. Am. J. Clin. Nutr., 71, p 28-35.

[Reference 7] Hur SH. 1996. Critical review on the microbiological standardization of salt-fermented fish product. J. Korean Soc. Food Sci. Nutr., 25, p885-891

8 Kobatake Y, Saito M, Kuroda K, Kobayashi S, Innami S. 1987. Influence of fish consumption on serum lipid and lipid peroxide concentrations in middle aged subjects. J Japan Soc Nutr & Food Sci 40, p 103-110.

Kusama H, Nishiyama M and Ikeda S. 1988. Pharmacological investigation of bezafibrate a hypolipidemic agent (1). Effects of bezafibrate on normal and experimental hyperlipidemia in rats. Nippon yakurigaku Zasshi. 92, p 175-180.

Lind L, Vessby B and Sundstrom J. 2006. The apolipoprotcin B / AI ratio and the metabolic syndrome independently predict risk for myocardial infarction in middle-aged men. Arterioscler. Thromb. Vasc. Biol., 26, p406-410.

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Noma A, Matsushita S and Komori T. 1986. High-density lipoprotein cholesterol levels of very old people in the diagnosis of dementia. Oxford Journals 15, p 267-270.

Richmond W. 1976. Use of cholesterol oxidase for assay of total and free cholesterol in serum by continuous flow analysis. Clin. Chem., 22, p 1579.

16 Wout ZG, Pec EA, Maggiore JA, Willams RH, Palichara P and Johnston TP. 1992. Poloxamer 407-mediated changes in plasma cholesterol and triglycerides following intraperitoneal injection to rats. Paenter Sci. Technol. 46, p192-200.

Yagi K. 1987. Lipid peroxides and human diseases. Chemistry and Physics of Lipids 45, p 337-342.

[Document 18] Lee Ki-wan et al. 4, 100 Years of Koreans' Dietary Life Evaluation (Ⅰ), Shinkwang Publishing Co., 1998

[Document 19] Kim Eun-kyung et al. 4, Life Cycle Nutrition. Shinkwang Publishing Co., 2005

[20] Cho Seong-hee, Geology and Atherosclerosis, Korean Journal of Nutrition and Nutrition 23 (1) , pp.170-179, 1994

[Reference 21] Korea Food Industry Association Food Research Institute, A Study on the Relationship between Nutrition and Special Diseases, 1988

22 Eddy, NB et al ,, Synthetic analgesics. II. Dithienylbutenyl- and dithienylbutylamines. J Pharmacol Exp Ther. 107 (3) , pp. 385-393, 1953

23, D ^, Amour, FE, et al ,, A method for determining loss of pain sensation. J. Pharmacol. Exp. Ther. 72 , p.74, 1941

24 Imad Damaj, M. et al ,, Tolerance to the antinoceptive effect of epibatine after acute and chronic administration in mice. Euorpian J Pharmacol. 300 , pp. 51-57, 1996

[Science 25] Kim Song Jeon, Kim Man Soo. Effect of ω-3 Fatty Acids on Serum Lipids in Cholesterol-treated Rats, Journal of the Korean Chemical Society, 1991

[26] Effects of Fish Oil Dose on Serum Lipids in Patients with Insulin-Independent Diabetes Mellitus, Korean Journal of Nutrition, 26 (6) , pp.672-679, 1993

Schoen FJ et al., Robbins pathologic basis of disease, 5 th ed . , pp. 473-484, 1994

[Ref. 28] Kook Seung-rae et al., Journal of Family Medicine, 18 (3) , pp.317-327, 1997

29 I. Ham et al., Kor. J, Herbology, 20 , pp. 45-52, 2005

30 H Lee et al., Kor. J. Anesthesiol, 40 , pp. 515-521, 2001

31 J Choi et al., J. Kor. Pharm. Sci., 18 , pp. 240-241, 1988

[32] Kim KK et al., J. Kor. Pharm. Sci., 28 , pp. 15-23, 1998

33 Nash VJ et al., Pharmacotherapy, 16 , pp. 10-15, 1996

34 Stellato C. et al., Br. J. Anaesth., 67 , pp. 751-758, 1991

Rhee, S.K., et al ,, Lipid Content of Different Section and Fatty Acid Composition of Mackerel, Pacific Saury and sardine, pp. 82-88, 2001

[Reference 36] Kim So-mi et al., Story of Korean Fish that Everyone Should Know, Hyo-il, 2002

37, Oh, S.H., Kim, D.J, .The Change in Content of Constitutive Lipid and Fatty Acid of Pacific Saury during Natural Freezing Dry (Kwa Mae Kee), Korean J. Food & Nutrition, pp.239-252, 1995

Disease is a part of human life, and its pattern has changed with age. The economic development and high industrialization, rapid population growth and densification, environmental and health hygiene, and the development of new therapies that our society has experienced over the past 100 years have changed the disease structure of our people more than ever before. Brought. Korea's disease structure is shifting from infectious diseases to adult diseases, and the morbidity and mortality levels are changing accordingly (Kiwan et al. In terms of sign structure of Koreans, tuberculosis, bronchitis, gastroenteritis, etc. occupied the upper ranks before the 1950s. However, in 1997, the number of signs of death was circulatory disease (hypertensive disease, cerebrovascular disease, ischemic heart disease). , Arteriosclerosis, etc., accounting for 23.4% of all deaths (Eun-Kyung Kim et al. 4, Life Cycle Nutrition. Shin-Kwang Publisher, 2005). Cardiovascular disease is a major cause of premature mortality worldwide and is a multifactorial disease caused by genetics and other environmental factors. It has been reported to be closely related to lipid nutrition (Cho Sung-Hee, Lipid and Arteriosclerosis, Korea Nutrition) Korean Journal of Food Science and Technology 23 (1) , pp.170-179, 1994; Korean Food Industry Association Food Research Institute, A Study on the Relationship between Nutrition and Special Diseases, 1988).

Hyperlipidemia is the case when the concentration of serum lipids is higher than normal (Illingworth, DR et al ,, Atherosclerosis, 4 , p. 270, 1984). These symptoms are due to increased synthesis of triglycerides in the small intestine and triglycerides in the liver. Increased synthesis, decreased HDL-cholesterol synthesis, increased VDL-cholesterol synthesis and secretion (Eddy, NB et al ,, Synthetic analgesics. II.Dithienylbutenyl- and dithienylbutylamines.J Pharmacol Exp Ther. 107 (3) , pp. 385 -393, 1953; D ^, Amour, FE, et al ,, A method for determining loss of pain sensation.J. Pharmacol.Exp. Ther. 72 , p.74, 1941; Imad Damaj, M. et al ,, , Tolerance to the antinoceptive effect of epibatine after acute and chronic administration in mice.Europian J Pharmacol. 300 , pp.51-57, 1996) or due to tissue damage following lipid peroxidation (Kim Song-jeon, Kim Man-soo.ω-3 Effects of Fatty Acids on Serum Lipids in Cholesterol-treated Rats, Journal of the Korean Chemical Society, 1991; Non-dependent effects the amount of fish oil administered in diabetic patients on serum lipids, Korea Nutrition Society, 26 (6), pp.672-679, 1993).

In hyperlipidemia, the major components of increased serum lipid components are composed of fat-soluble substances such as cholesterol, triglycerides, phospholipids, and free fatty acids, and hypercholesterinemia, depending on which of these lipid substances increases mainly. It is called hypertriglyceridemia. Increased serum cholesterol and triglycerides are the most common causes of hyperlipidemia. Accumulation of excess fat causes blood circulation disorders and microcirculation failure, resulting in atherosclerosis, ischemic heart disease, cerebral infarction, hypertension, obesity, diabetes, etc. (Schoen FJ et al., Robbins pathologic basis of disease, 5 th ed . , pp. 473-484, 1994).

Cholesterol is produced mainly in the liver and is present in the blood in the form of small round particles called lipoproteins, which carry cholesterol throughout the body. There are two types of lipoproteins, low density lipoprotein (LDL) and high density lipoprotein (HDL), and because high density lipoproteins carry cholesterol from other tissues to the liver, a lot of high density lipoproteins remove cholesterol from blood vessels. On the other hand, low-density lipoproteins are mainly produced by the liver and transport cholesterol to other tissues of the human body, so a lot of low-density lipoproteins accumulate a lot of cholesterol in blood vessels to promote arteriosclerosis, and about 70% of blood cholesterol is present as low-density lipoproteins, which are bad cholesterol.

In fact, cholesterol is an essential ingredient for normal functioning of the human body, a nutrient necessary for making cells, and a component of various hormones such as corticosteroids, male hormones, and female hormones. do. In addition, cholesterol is a nutrient necessary for the human body such as being used as a constituent of biological membranes and as a starting material for hormonal synthesis. However, excessive cholesterol intake is known to accumulate in the blood vessels and cause heart disease, and there is no preventive method except low-cholesterol diet, and taking drugs such as cholesterol-lowering drugs is effective. Use is extremely limited due to reasons such as causing side effects such as liver dysfunction.

Chitosan, phytosterol, inositol, pectin, etc. are known to lower blood cholesterol in the human body, but the effects and metabolic mechanisms are not clear when phytosterol is excluded. not. Phytosterol, a plant sterol due to its structural similarity to cholesterol, has already been identified as a mechanism for inhibiting cholesterol absorption metabolism in the body through competition with low-density lipoprotein-cholesterol, which is harmful to the human body. As a food additive, the US Food and Drug Administration (FDA) Has been approved.

Hyperlipidemia drugs are used to lower levels of excess blood lipids, especially cholesterol and triglycerides. Major drugs used in lipid metabolism include statins, bile acid blockers and fibric acid derivatives, each of which acts as a different mechanism. The choice of therapeutic agents for hyperlipidemia may be a combination of these drugs, depending on the type of lipoproteins that have been increased, and they require long-term oral daily use. These drugs effectively lower cholesterol and blood lipid levels, but have the disadvantage of having side effects. Statins can cause nausea, headache, abdominal pain and diarrhea or constipation, which can cause muscle inflammation, and bile acid blockers can reduce the intestinal absorption of vitamins A, D, and K. And fibric acid derivatives are unsuitable drugs for kidney disease, liver disease or gallbladder disease. Therefore, there is an increasing demand for the development of medicines and functional foods containing natural products to replace these preparations (Kook Seung-rae et al., 18 (3) , pp.317-327, 1997).

Atherosclerosis causes vascular diseases such as stroke and coronary artery disease. In particular, angina and acute myocardial infarction caused by coronary artery disease have increased significantly over the last 20-30 years due to rapid social and economic development and westernized lifestyle. Arteriosclerosis is the second most common circulatory disease after hypertension, and it is one of the most important diseases in national health, with cancer accounting for a large portion of deaths. Therefore, the importance of research on the pathogenesis and treatment of atherosclerosis is increasing.

There are many causes of atherosclerosis, but elevated plasma lipids, particularly plasma cholesterol and neutral lipids, are known as one of the most important risk factors.

Hyperlipidemia is an important risk factor for atherosclerosis and is a clinically important condition that causes major deaths such as ischemic heart disease and cerebrovascular disorders. Atherosclerosis prevention is known to be associated with improved lipid and hyperlipidemia.

The pathological model of experimental hyperlipidemia is divided into exogenous model and endogenous model. Exogenous hyperlipidemic condition models include hypercholesterolemia-induced models caused by high cholesterol dietary load, that is, hyperlipidemia by administration of vitamin D, cholesterol, olive oil, corn oil, etc., and endogenous hyperlipidemia models include fructose administration and WR. Models by administration of -1339 (Tripton WR-1339) (Ham IH et al., Kor. J, Herbology, 20 , pp. 45-52, 2005). Among them, Poloxamer 407 is an anesthetic emulsifier (Lee HH et al., Kor. J. Anesthesiol, 40 , pp. 515-521, 2001), poorly soluble drug solubilizer (Choi JY et al., J. Kor. Pharm. Sci., 18 , pp. 240-241, 1988), skin ointments (Kim KK et al., J. Kor. Pharm. Sci., 28 , pp. 15-23, 1998), and the like. However, when administered in humans, lipids are increased, and in particular, triglycerides are increased, causing hyperlipidemia. Free fatty acids are produced in adipocytes for at least 24 hours after poloxamer injection (Nash VJ et al., Pharmacotherapy, 16 , pp. 10-15, 1996), and the action of lipoprotein lipase (LPL) Decreases the rate of degradation of triglycerides that interfere with it (Stellato C. et al., Br. J. Anaesth., 67 , pp.751-758, 1991), and increases blood cholesterol and triglycerides in the liver. This is because it lowers the activity of hydroxy-3-methylglutaryl coenzyme A (HMG-CoA; 3-hydroxy-3-methylglutaryl CoA) (Wout GM et al., J. Paren. Sci. Technol., 46 , pp. 192-200, 1992).

Lipid peroxidation in the blood is known to cause cytotoxicity and cause aging and pathologies of various diseases. Fatty Acid Composition of Mackerel, Pacific Saury and sardine, pp. 82-88, 2001; Kim So Mi et al., Hyo Il, 2002; Oh, SH, Kim, DJ, .The Change in Content of Constitutive Lipid and Fatty Acid of Pacific Saury during Natural Freezing Dry (Kwa Mae Kee), Korean J. Food & Nutrition, pp.239-252, 1995).

Fermented foods have been widely used in Korea, Japan and Southeast Asia, where rice is a staple food. The origin of the literature on salted salted saltfish in Korea was the first record of Samguk Sagi, which was contained in the waste white goods when the queen was greeted by King Shilla three years (683). Salted seafood was used in the manufacturing process, and since then, it has been changed in various forms as it is divided into salted sea salt (now salted salted fish) and salt, malt, and cooked grains (fish snails). .

Salted seafood is a traditional Korean fermented food product that suppresses the growth of decayed bacteria by salting fish and shellfish and decomposes meat by the action of autodigestive enzymes or microorganisms.The manufacturing process is simple and no special manufacturing equipment is required. After ripening, the product has a unique rich flavor and has been widely used as a seasoning material for side dishes or kimchi from old days to today. However, since salted salt is traditionally used in high concentrations of salt, it has been avoided by consumers since it is found that the main ingredient of salt is one of the causes of adult diseases, and it is urgently needed for products of salted salted salted salt.

Anchovy salt, salted fish paste, canary fish sauce, and anchovy salted fish sauce in other regions are at least 20% high-fat foods, while seasoned salted seafood such as shrimp, flatfish, pollack, squid and shrimp chops are made from Sokcho. It shows a very low salt concentration of ~ 4.9%, and without the concern of adult diseases such as high blood pressure caused by salt, rather, a large amount of functional free amino acids, GABA, conjugated fatty acids produced during fermentation are produced and added to the functionality of the seafood itself. This is expected to be further enhanced.

Accordingly, the present inventors have continuously studied the effects of obesity or hyperlipidemia and the prevention and treatment of atherosclerotic cardiovascular diseases by using shrimp salt powder, shrimp salt polar solvent soluble extract, and polar solvent insoluble extract residues. Poloxamer-407 or Triton WR- 1339 administration was confirmed to reduce blood triglyceride and cholesterol content in hyperlipidemia-induced animal model, and to reduce liver lipid and fecal lipid content in animal model induced hyperlipidemia by high-cholesterol diet. In addition, it has been confirmed to reduce cholesterol, phospholipids, lipid peroxide and Hydroxyl radical content, and enhance SOD activity in serum, and to confirm that the present invention contains a large amount of conjugated fatty acid which is known to be excellent in anti-obesity, anti-cancer and antioxidant effects. To complete.

In order to carry out the above object, the present invention provides a pharmaceutical composition for the prevention and treatment of obesity or hyperlipidemia and atherosclerotic vascular disease containing shrimp salt powder, shrimp salt polar solvent soluble extract or polar solvent insoluble extract residue as an active ingredient.

In addition, the present invention provides a dietary supplement for the prevention and improvement of obesity or hyperlipidemia and atherosclerotic vascular disease containing shrimp salt powder, shrimp salt polar solvent soluble extract or polar solvent insoluble extract residue as an active ingredient.

Shrimp paste powder as defined herein comprises a commonly distributed product form or a dry powder thereof, preferably lyophilized powder form.

Also, the soluble polar solvent soluble extract as defined herein is a solvent selected from water including purified water of shrimp powder, a lower alcohol having 1 to 4 carbon atoms or a mixed solvent thereof, preferably a water and ethanol mixed solvent, more preferably 50- Extracts soluble in 99% water and ethanol mixed solvents.

In addition, the shrimp salt polar solvent insoluble extraction residue defined herein is a solvent selected from water including purified water of shrimp powder, a lower alcohol having 1 to 4 carbon atoms or a mixed solvent thereof, preferably a water and ethanol mixed solvent, more preferably Contains insoluble residue in 50-99% water and ethanol mixed solvent.

Hyperlipidemia and atherosclerotic vascular diseases as defined herein are specifically hyperlipidemia, arteriosclerosis, heart failure, hypertensive heart disease, arrhythmia, congenital heart disease, myocardial infarction, angina pectoris, stroke or peripheral vascular disease, preferably hyperlipidemia or arteriosclerosis to be.

Hereinafter, a method of obtaining shrimp salt powder, shrimp salt polar solvent soluble extract or polar solvent insoluble extract residue of the present invention will be described in detail.

For example, the first step of immersing the shrimp in a seasoning solution for 1 hour to 60 hours, preferably 10 to 50 hours after washing and washing the shrimp; Red pepper powder, sugar, garlic, starch syrup, etc. are added to the seasoned shrimp, and the shrimps are cooked at low temperature for 1 hour to 60 hours, preferably 10 hours to 50 hours at 0 ° C. to 50 ° C., preferably 5 ° C. to 45 ° C. Preparing a second step; Shrimp chopped powder of the present invention can be obtained through the manufacturing process of the third step of lyophilizing the prepared chopped shrimp.

In the first step, the seasoning liquid used in the present invention has a relative compounding weight ratio (w / w) of 11.4% salt, 4.5% seasoning powder, 2% sorbitol, and 2% alcohol 5 to 20: 3 to 10: 1 to 3 1 to 3, preferably 5 to 15: 3 to 8: 1 to 3: 1 to 3, characterized in that the composition is composed of a seasoning liquid mixed.

In the second step, the seasoned shrimp, red pepper powder, sugar, garlic, syrup, etc., preferably, the relative compounding weight ratio (w / w) of red pepper powder: sugar: garlic: syrup is 1-15: 1-10: 1: 1 ? 3, preferably 1? 10: 1? 5: 1: 1? 2, and more preferably 1? 9: 1? 4: 1: 1? 1.5.

In addition, the shrimp salt polar solvent soluble extract and the polar solvent insoluble extract residue are, for example, about 1 to 100 times the weight of the powder, preferably 1 to 10 times the volume (w / v) in the shrimp salt powder obtained by the above-described manufacturing method. A solvent selected from water containing purified water, a lower alcohol having 1 to 4 carbon atoms, or a mixed solvent thereof, preferably water, ethanol or a mixed solvent thereof, at 0 ° C. to 100 ° C., preferably at 20 ° C. to 50 ° C. Decompression filtration using extraction methods such as cold needle extraction, hot water extraction, reflux circulation extraction, ultrasonic extraction or pressure extraction for minutes to 1 hour, preferably 15 minutes to 1 hour, preferably by performing ultrasonic extraction Through the polar solvent soluble extract and shrimp solvent insoluble extract residues, preferably, ethanol soluble extract except for the polar solvent soluble extract Shrimps and ethanol can be obtained a water-insoluble extraction residue, respectively concentrated and freeze-dried to afford the shrimp polar solvent soluble extract and polar solvent-insoluble extraction residue, respectively.

Accordingly, the present invention provides a pharmaceutical composition for the prevention and treatment of obesity or hyperlipidemia and atherosclerotic vascular disease, comprising shrimp salt powder, shrimp salt polar solvent soluble extract or polar solvent insoluble extract residue obtained as the active ingredient. .

The pharmaceutical composition of the present invention comprises from 0.1 to 50% by weight of the shrimp powder, shrimp salt soluble extract or polar solvent insoluble extract residue based on the total weight of the composition.

However, the composition is not limited thereto, and may vary depending on the condition of the patient, the type of disease, and the progress of the disease.

Shrimp salt powder, salt soluble polar solvent soluble extract or polar solvent insoluble extract residue of the present invention is a drug that can be used with confidence even for long-term use for the purpose of prevention because there is little toxicity and side effects.

The compositions of the present invention may further comprise suitable carriers, excipients and diluents conventionally used in the manufacture of pharmaceutical compositions.

The composition of the present invention may be formulated in the form of powders, granules, tablets, capsules, suspensions, emulsions, syrups, aerosols and the like, oral preparations, suppositories and sterilized injection solutions, Examples of carriers, excipients and diluents that can be included in the composition containing the extract include lactose, dextrose, sucrose, sorbitol, mannitol, xylitol, erythritol, maltitol, starch, acacia rubber, alginate, gelatin, calcium phosphate, calcium silicate , Cellulose, methylcellulose, microcrystalline cellulose, polyvinylpyrrolidone, water, methylhydroxybenzoate, propylhydroxybenzoate, talc, magnesium stearate and mineral oil. When formulated, diluents or excipients such as fillers, extenders, binders, wetting agents, disintegrating agents, and surfactants are usually used. Solid preparations for oral administration include tablets, pills, powders, granules, capsules, and the like, and the solid preparations may include at least one excipient such as starch, calcium carbonate, sucrose in the extract. ) Or lactose, gelatin and the like are mixed. In addition to simple excipients, lubricants such as magnesium stearate talc are also used. Examples of the liquid preparation for oral use include suspensions, solutions, emulsions, and syrups. In addition to water and liquid paraffin, simple diluents commonly used, various excipients such as wetting agents, sweeteners, fragrances, preservatives and the like may be included . Formulations for parenteral administration include sterilized aqueous solutions, non-aqueous solutions, suspensions, emulsions, freeze-dried preparations, and suppositories. As the non-aqueous solvent and suspending agent, propylene glycol, polyethylene glycol, vegetable oil such as olive oil, injectable ester such as ethyl oleate, and the like can be used. As the base of the suppository, witepsol, macrogol, tween 61, cacao butter, laurin butter, glycerogelatin and the like can be used.

The preferred dosage of the composition of the present invention varies depending on the condition and the weight of the patient, the degree of disease, the type of drug, the route of administration and the period of time, but can be appropriately selected by those skilled in the art. However, for the desired effect, the shrimp and shrimp of the present invention is preferably administered at 0.5 g / kg to 5 g / kg, preferably 1 g / kg to 3 g / kg per day. The administration may be carried out once a day or divided into several doses. Thus, the dosage amounts are not intended to limit the scope of the invention in any manner.

The composition of the present invention can be administered to mammals such as rats, mice, livestock, humans, etc. by various routes. All modes of administration may be expected, for example, by oral, rectal or intravenous, intramuscular, subcutaneous, intra-uterine or intracerebroventricular injections.

In addition, the present invention provides a dietary supplement for the prevention and improvement of obesity or hyperlipidemia and atherosclerotic vascular disease, comprising shrimp salt powder, shrimp salt polar solvent soluble extract or polar solvent insoluble extract residue obtained as the active ingredient. do.

The composition comprising shrimp salt powder, shrimp salt polar soluble extract or polar solvent insoluble extract residue of the present invention can be used in a variety of drugs, foods and beverages for the prevention and improvement of obesity or hyperlipidemia and atherosclerotic vascular disease. The foods to which the shrimp paste and shrimp of the present invention can be added include, for example, various foods, beverages, gums, teas, vitamin complexes, health supplements, etc., and are in the form of powders, granules, tablets, capsules, or beverages. Can be used.

The shrimp salt powder, shrimp salt polar soluble extract or polar solvent insoluble extract residue of the present invention may be added to food or beverage for the purpose of preventing and improving obesity or hyperlipidemia and atherosclerotic vascular disease. At this time, the amount of the shrimp and shrimp in the food or beverage is generally added to the health food composition of the present invention 1 to 5% by weight of the total food weight, the health beverage composition is 0.02 to 10 g based on 100 ml, Preferably it can be added in the ratio of 0.3-1 g.

The health beverage composition of the present invention, in addition to containing the salted shrimp and shrimp as essential ingredients in the indicated ratio, there is no particular limitation on the liquid component, and may contain various flavors or natural carbohydrates as additional ingredients, such as ordinary drinks. have. Examples of the above-mentioned natural carbohydrates include monosaccharides such as disaccharides such as glucose and fructose such as maltose, sucrose and the like and polysaccharides such as dextrin, cyclodextrin and the like Sugar, and sugar alcohols such as xylitol, sorbitol, and erythritol. As flavoring agents other than those described above, natural flavoring agents (tauumatin, stevia extract (e.g., Rebaudioside A, glycyrrhizin, etc.) and synthetic flavoring agents (saccharin, aspartame, etc.) can be advantageously used. The proportion of said natural carbohydrates is generally about 1-20 g, preferably about 5-12 g per 100 mL of the composition of the present invention.

In addition to the above-mentioned composition, the composition of the present invention can be used as a flavoring agent such as various nutrients, vitamins, minerals (electrolytes), synthetic flavors and natural flavors, coloring agents and intermediates (cheese, chocolate etc.), pectic acid and its salts, Salts, organic acids, protective colloid thickening agents, pH adjusting agents, stabilizers, preservatives, glycerin, alcohols, carbonating agents used in carbonated beverages and the like. In addition, the compositions of the present invention may contain flesh for the production of natural fruit juices and vegetable beverages. These components can be used independently or in combination. The proportion of such additives is not so critical, but is generally selected in the range of 0 to about 20 parts by weight per 100 parts by weight of the composition of the present invention.

Shrimp salt powder, soluble polar solvent soluble extract or polar solvent insoluble extract residue of the present invention reduces lipid content in liver tissue and feces in animal models causing hyperlipidemia, triglyceride, cholesterol, phospholipid, lipid peroxide and Hydroxyl in serum It has been confirmed to reduce the radical content and enhance the SOD activity in the serum, and it has been found to contain a large amount of conjugated fatty acid, which is known to be excellent in anti-obesity, anti-cancer, and antioxidant effects, preventing obesity or hyperlipidemia and atherosclerotic vascular disease And pharmaceutical compositions and nutraceuticals useful for the treatment.

Hereinafter, the present invention will be described in detail by reference examples, examples and experimental examples.

However, the following Reference Examples, Examples and Experimental Examples are merely illustrative of the present invention, and the content of the present invention is not limited to the following Reference Examples, Examples and Experimental Examples.

Example  1. Preparation of Shrimp Powder, Polar Solvent Soluble Extract and Insoluble Residue

1-1. Preparation of Lyophilized Products

Shrimp taken from Sokcho were washed, sorted and selected. Shrimp was seasoned with salt 11.4%, seasoned powder 4.5%, sorbitol 2%, and 2% alcohol. ~ 10%), sugar (1 ~ 10%), garlic (1 ~ 10%), starch syrup (1 ~ 10%) was added, and aged for 48 hours at 0 ~ 10 ℃ to prepare a shrimp chop.

The prepared shrimp chopped at -70 ℃ using an ultra-low temperature freezer (DFS520, Ilshin Lab, Korea), and then freeze-dried for 48 hours with a vacuum freeze dryer (PVIFD30A, Korea Ilshin Lab) (hereinafter referred to as "SR-D"). And stored as it is at -40 ℃ was used as a sample of the following experiment.

1-2. Preparation of Ethanol Extracts and Insoluble Residues

Vacuum-dried samples (200 g dry weight) were placed in a 1,000 mL Erlenmeyer flask, followed by adding 95% ethanol 4 times (w / v) of the sample volume, followed by sonication at 30 ° C for 30 minutes (power SONIC 520 HWASHIN). Ultrasonic extraction and filtration under reduced pressure separated the extract (hereinafter referred to as "SRE") and the residue (hereinafter referred to as "SRER").

The residue was stored at -20 ° C. after removing ethanol at room temperature, and the ethanol extract was used in the experiment while removing ethanol at 40 ° C. with a reduced pressure concentrator (BUCHI Rotavator; R-200).

Reference Example  1. Preparation for experiment

1-1. Experimental Animal, Experimental  Configuration

Quarantine and purified for 1 week after purchasing 4 weeks old male from SPF 25 ± 3 g ICR male mice and 140 ± 10 g Sprague Dawley (SD) rats (Hyochang Science Co., Ltd.). After breeding, only healthy animals were used for the experiment. The breeding environment of this test was set at 22 ± 3 ℃, 50 ± 10% relative humidity, and 12 hours of illumination time (07: 00 ~ 19: 00). ). Feed was freely ingested for drinking water, which was a solid feed for animals (Central Experimental Animal, Seoul). 24 hours before the experiment time only watering and fasting. At this time, the experimental animals were treated within a certain time (10:00 AM ~ 12:00 AM) in consideration of the daily variation of enzyme activity.

1-2. Sample  Produce

Using 4% tween 80 diluted shrimp salt powder, shrimp salt ethanol extract and ethanol extract residue with physiological saline, the samples were administered to each experimental group at 100, 200 mg / kg doses for 4 weeks using oral needle zonde.

1-3. Statistical analysis

The mean ± standard deviation of the three test results was shown. To test the homogeneity of variance, Duncan's multiple range test was used to determine statistical significance when the difference was less than 5% ( p <0.05). (Meaning that there is a statistically significant difference between the superscript alphabets in the data).

Experimental Example  1. Hyperlipidemia and lipid content measurement experiment

1-1. Poloxamer Hyperlipidemia with -407 administration

According to the method of Wout (Wout GM et al., 1992), poloxamer-407 (300 mg / kg) was dissolved in physiological saline in an ice bath on the last day of administration of the sample, and the mice were intraperitoneally administered and killed 24 hours later.

1-2. Triton WR - By 1339  Hyperlipidemia

According to the method of Kusama (Kusama, H et al., 1988), fasting for 16 hours prior to Triton WR-1339 administration, and then triton WR-1339 200mg / kg injected into the tail vein to induce hyperlipidemia and CO after 18 hours ₂ Blood was collected by anesthesia with gas.

1-3. Cholesterol  Induction of induced hyperlipidemia

The induction of dietary cholesterol hyperlipidemia in experimental animals was induced by breeding a preparation sample containing sodium cholate and cholesterol for 6 weeks (see Table 1).

Ingredient Basal diet
(%) Hyperlipidemic Diet
(%) Casein 20.0 20.0 DL-Methionine 0.3 0.3 Corn starch 15.0 15.0 Sucrose 50.0 34.5 Corn oil 5.0 - AIN-mineral Mixture ¹⁾ 3.5 3.5 AIN-vitamin Mixture ²⁾ 1.0 1.0 Fiber ³⁾ 5.0 5.0 Choline bitartate 0.2 0.2 Beef tallow - 20.5 ¹⁾ Mineral mixture contain the following (g / kg diet): calcium phosphate dibasic 500.0, sodium chloride 74.0, potassium citrate monohydrate 220.0, potassium sulfate 52.0, magnesium oxide 24.0, magnesium carbonate 3.5, ferric citrate 6.0, zinc carbonate 1.6, cupuric carbonate 0.3, potassium iodate 0.01, chromium potassium sulfate 0.55, sucrose, finely powered make 1,000
²⁾ Vitamin mixture (g / kg diet): thiamine HCl 0.6, biotin 0.02, riboflavin 0.6, cyanocobalamine 0.001, pyridoxine HCl 0.7, retinyl acetate 0.8, nicotinic acid 3.0, DL-tocopherol 3.8, Ca-pantothenate 1.6, 7-dehydrocholesterol 0.0025 , folic acid 0.2, methionine 0.005, sucrose, finely powered make 1,000
³⁾ Cellulose: Sigma Co. LTD., USA

1-4. Serum and Enzyme  pharmacy

After the sample was injected, the animal was lightly anesthetized with CO ₂ , and blood was collected from the abdominal aorta. The collected blood was left for 30 minutes and centrifuged at 3,000 rpm for 10 minutes to separate serum and lipid, lipid peroxide, hydroxyl radical. The content and superoxide dismutase activity were measured.

1-5. Body weight and fat tissue weight measurement

Body weight change was measured every week from the start of the experiment, the weight of the adipose tissue was calculated by taking the fat around the abdominal cavity and testicles.

1-6. Liver tissue  And Feces  Heavy lipid content measurement

Liver tissue was weighed and stored frozen at -70 ℃, feces collected for the last 4 days. Triglyceride and cholesterol were measured by Folch et al. In other words, the stools were lyophilized and ground to be powdered. The liver tissues were cut and then ground with a teflon homogenizer. 10 times the amount of solvent (chloroform: methanol = 2: 1) was added to the sample, and the lipids were repeatedly extracted. The filtrate was put in a water container and concentrated under reduced pressure to obtain lipids. Methanol was added thereto to dissolve well, and then quantified using an enzyme kit (AM 202-K, Asan).

1-7. Total cholesterol  Content measurement

Experiments were carried out using a kit (AM 202-K, Asan) prepared by the enzyme method of Richmond (Richmond W et al., 1976).

Enzyme reagents (containing 20.5 U / L cholesterol esterase, 10.7 U / L cholesterol oxidase, and 1.81 g / L sodium hydroxide) were dissolved in an enzyme reagent solution (potassium phosphate monobasic 13.6 g / L, phenol 1.88 g / L). 3.0 ml of the enzyme solution prepared in 20 μl of the sample was added to the dissolved solution, followed by incubation at 37 ° C. for 5 minutes, and the absorbance was measured at a wavelength of 500 nm using the reagent blank as a control. The blood content was expressed in mg / dl according to the standard calibration curve.

1-8. Triglyceride  Content measurement

Experiments were performed using a kit (AM 157S-K, Asan) prepared according to the method of McGowan (McGrowan Mw et al., 1983). Enzyme reagent (containing lipoprotein lipase 10800U, glycerol kinase 5.4U, peroxidase 135000U, and L-α-glycero phosphooxidase 160U) in ice cold phase was dissolved in enzyme reagent [N, N-bis (2-hydroxyethyl) -2-aminomethane sulfonic acid 0.427 g / dl containing], 3.0 ml of the enzyme solution prepared in 20 µl of the sample was added thereto, and then incubated at 37 ° C for 10 minutes, and the absorbance was measured at a wavelength of 500 nm using the reagent blank as a control. The blood content was expressed in mg / dl according to the standard calibration curve.

1-9. Phospholipid  Content measurement

Experiments were carried out using a kit (Iatron Chem. Co.) prepared by the enzyme method of Chen (Chen PS et al., 1956). In an ice cold solution, 20 µl of enzyme reagent (containing phospholipase 3.9U, choline oxidase 5.6U, peroxidase 3.6U, 4-aminoantipyrine 0.3252 mg) dissolved in enzyme reagent solution [containing tris (hydroxymethyl) -aminomethane 6.057 mg]. 3.0 ml of the prepared enzyme solution was added, followed by incubation at 37 ° C. for 20 minutes to measure absorbance at a wavelength of 500 nm. The content was expressed in mg / dl according to the standard calibration curve.

1-10. High density lipoprotein - cholesterol ( HDL -C) content determination

The experiment was carried out using a kit (AM 203-K, Asan) prepared by the enzyme method of Noma (Noma A et al., 1986). 0.2 ml of sedimentation reagent (containing dextran sulfate 0.1% and magnesium chloride 0.1M) was added to 20 µl of serum and mixed well. The mixture was left at room temperature for 10 minutes and centrifuged at 3000 rpm for 10 minutes. 0.1 ml of the supernatant was mixed well with 3.0 ml of enzyme solution, incubated at 37 ° C. for 5 minutes, and the absorbance was measured at a wavelength of 500 nm using the reagent blank as a control. The content was expressed in mg / dl according to the standard calibration curve.

1-11. LDL -And VLDL - chlesterol  Content measurement

Low density lipoprotein-cholesterol (LDL-C) content was calculated by Equation 1 according to the method of Fridewald (Friedwald, WT et al., 1972).

The measurement of VLDL (Very low density lipoprotein) content was calculated by the formula of serum total cholesterol-(HDL-C + LDL-C). Atherosclerotic index (AI) was calculated by the formula (serum cholesterol-HDL-C) / HDL-C.

1-12. Blood Lipid peroxide  Content measurement

According to the method of Yagi (Yagi K. 1987), add 4.0 ml of 1 / 12N H ₂ SO ₄ to 20 µl of serum, mix 0.5 ml of 10% phosphotungstic acid, and leave it at room temperature for 5 minutes, and then centrifuge to remove the serum. The protein was taken out and centrifuged again with 2.0 ml of 1 / 12N H ₂ SO ₄ and 0.3 ml of 10% phosphotungstic acid. 1.0 ml of a solution of 4.0 ml of distilled water, a mixture of 0.67% thiobarbituric acid, and acetic acid in a 1: 1 mixture was added thereto. After centrifugation for a minute, the resulting red n-BuOH was taken and the absorbance was measured using a spectrofluorometer (Ex: 515 nm, Em: 553 nm). Tetraethoxypropane 0.5nmole was reacted with the standard solution in the same manner to measure the absorbance, and the serum lipid peroxide content was calculated by Equation 2 below.

1-13. Blood Hydroxyl radical  Content measurement

According to the method of Kobatake (Kobatake Y et al., 1987), 34.8 μl of serum was added to 0.54 M NaCl, 0.1 M potassium phosphate buffer (pH 7.4), 10 mM NaN ₃ , 7 mM deoxyribose, 5 mM ferrous ammonium sulfate and 333.3 μl of distilled water. The mixture was added so as to mix well in the vortex and allowed to stand at 37 ° C for 15 minutes. 67 μl of serum was taken and mixed with 75 μl of 8.1% sodium dodecyl sulfate, 500 μl of 20% acetic acid and 25 μl of distilled water. 333 μl of 1.2% thiobarbituric acid was added thereto, followed by heating in a water bath (100 ° C.) for 30 minutes, cooling at room temperature, and centrifugation at 700 × g for 5 minutes to measure absorbance at a wavelength of 532 nm. The content of hydroxyl radical (nmole / mg protein) was quantified by the calibration curve.

1-14. Blood Superoxide dismutase ( SOD Activity measurement

It was quantified according to the method of Mirsa and Fridovich (Mirsa, HP and Fridovich, I., 1972). Serum was added to a certain amount of reaction solution (1 mmol / L adrenalin (pH 2), 50 mmol / L glycin (pH 10.2)) and reacted for 3 minutes at 30 ° C., and the amount of adrenochrome produced at 480 nm was measured. Enzyme activity was expressed as U / g protein of superoxide dismutase. One unit of SOD was calculated as 50% inhibition of adrenochrome production.

Protein quantification and statistical processing

Protein content was measured using bovine serum albumin (Sigma, Fr. V) as a standard according to the method of Lowry (Lowry OH., 1951). The results obtained in this experiment were expressed as mean ± standard deviation, and statistical significance was verified by Duncan's multiple range test.

2. Experimental results

2-1. Poloxamer -407 and Triton WR Efficacy on Hyperlipidemic Rats Induced by -1339 and

Poloxamer-407 and Triton WR-1339 have been reported to inhibit cell lipase activity, increase triglyceride and LDL in the blood, and increase the concentrations of high molecular weight Apo B, free and ester-bound cholesterol, phospholipids and fatty acids. (Hayashi et al., 1982). After inducing hyperlipidemia, the concentration of triglyceride and total cholesterol were observed by treating shrimp with different concentrations.

In the case of inducing hyperlipidemia with Poloxamer-407, the triglyceride and total cholesterol concentrations were significantly decreased in the group treated with high concentration of shrimp (200mg / kg) compared to the hyperlipidemia group.

When triton WR-1339 was used to induce hyperlipidemia, the triglyceride and total cholesterol concentrations in the high-fat shrimp group (200 mg / kg) decreased by 33% and 27% in the shrimp group compared to the hyperlipidemic group. A significant decrease was found.

The results of this experiment showed that the fat component, which is a trace component rather than the protein component that occupies most of shrimp, is a key compound in rats induced with Poloxamer-407 and Triton WR-1339 (see Tables 2 and 3).

Treatment Dose
(mg / kg) Triglyceride T-Cholesterol mg / dl Normal 98.7 ± 20.6 ^c 65.8 ± 16.4 ^d Poloxamer-407 1347.6 ± 213.5 ^a 859.4 ± 101.6 ^a  SR-D 100 1247.8 ± 189.2 ^a 814.2 ± 96.8 ^ab 200 893.5 ± 121.8 ^b 625.4 ± 73.1 ^c Mice were orally administered fermented shrimp (SR-D) daily for consecutive four weeks before poloxamer-407 induced hyperlipidemic state. Mice were sacrificed 24 hrs later for poloxamer-407 treated. Values are represent mean ± SD (n = 6).
Values sharing the same superscript letter are not significantly different each other (p <0.05) by Duncan ^, s multiple range test.

Treatment Dose
(mg / kg) Triglyceride T-Cholesterol mg / dl Normal 94.7 ± 19.4 ^c 68.7 ± 10.3 ^f Poloxamer-407 810.2 ± 89.6 ^a 230.5 ± 21.8 ^a  SR-D 100 721.4 ± 81.8 ^ab 171.3 ± 21.5 ^cd 200 694.3 ± 74.5 ^b 139.6 ± 20.9 ^e Mice were orally administered fermented shrimp (SR-D) daily for consecutive four weeks before triton WR-1339 (TWR) induced hyperlipidemic state. Mice were sacrificed 18 hrs later for triton TWR treated. Values are represent mean ± SD (n = 6). Values sharing the same superscript letter are not significantly different each other (p <0.05) by Duncan ^, s multiple range test.

2-2. Weight change

Body weight was measured every week from the start of the experiment, and the weight of the adipose tissue was measured after taking the abdominal cavity and peri testicular fat on the last day of the experiment is shown in Tables 4 and 5. As a result, 6 weeks of high cholesterol diet, hyperlipidemia induced 6 weeks of body weight was 321.6 ± 2.9g, which was about 15% of the normal group (6 weeks, 279.2 ± 1.8g). It was confirmed that the increase. In addition, as a result of administering Shrimp powder, Shrimp ethanol extract, Shrimp ethanol extract residue to hyperlipidemic test animals, it showed a significant weight loss effect compared to the control group. In addition, as shown in Table 5, as a result of administering Shrimp powder, Shrimp ethanol extract, Shrimp ethanol extract residue to hyperlipidemic test animals, the weight loss effect was found in both the abdominal cavity and testicular adipose tissue in both groups compared to the control group. (See Tables 4 and 5).

Treatment Dose
(mg / kg) 0  One 2 3 4 5 6 Weeks (g) Normal 135.7 ± 2.1 ^c 158.6 ± 1.5 ^c 179.6 ± 1.3 ^d 196.3 ± 2.6 ^g 231.9 ± 1.9 ^h 261.6 ± 3.7 ^g 279.2 ± 1.8 ^f Control 138.6 ± 1.7 ^ab 161.2 ± 2.8 ^abc 200.7 ± 1.5 ^b 241.8 ± 3.3 ^b 261.2 ± 3.2 ^c 301.7 ± 2.1 ^a 321.6 ± 2.9 ^b  SR-D 200 139.5 ± 1.6 ^a 160.4 ± 1.4 ^abc 209.5 ± 2.4 ^a 235.6 ± 2.1 ^d 256.7 ± 1.6 ^d 279.4 ± 1.8 ^e 304.3 ± 3.1 ^e  SRE 200 137.3 ± 2.0 ^abc 159.9 ± 1.5 ^abc 198.6 ± 1.8 ^b 230.3 ± 1.9 ^e 247.6 ± 1.7 ^f 265.3 ± 2.4 ^g 282.2 ± 1.6 ^f  SRER 200 136.8 ± 1.9 ^abc 161.3 ± 2.4 ^ab 210.7 ± 3.4 ^a 242.2 ± 1.8 ^b 268.5 ± 1.7 ^a 297.8 ± 3.8 ^ab 329.7 ± 3.5 ^a Rats were rendered obese by high fat diet for 6 weeks including a orally administered fermented shrimp daily for consecutive 4 weeks, and killed 24hr after the last treatment of fermented squid. The assay procedure was described in the experimental methods. Values are mean ± S.D. for five experiments. Values followed by the same letter are not significantly different (p <0.05).

Treatment Dose
(Mg / kg) Retroperitoneal Epididymal Mg / g body weight Normal 6.37 ± 1.16 ^e 7.84 ± 0.36 ^d Control 13.4 ± 1.07 ^a 11.8 ± 0.95 ^a   SR-D 200 9.32 ± 0.92 ^d 9.17 ± 0.39 ^c SRE 200 8.73 ± 0.99 ^d 8.97 ± 0.40 ^c SRER 200 10.8 ± 0.72 ^c 11.3 ± 0.47 ^ab The assay procedure was described in the experimental methods. Values are mean ± S.D. for five experiments. Values followed by the same letter are not significantly different (p <0.05).

2-3. Serum Lipid Composition Serum cholesterol  Content change and arteriosclerosis Number

To determine whether Shrimp extract was effective in inhibiting obesity, rats fed hyperlipidemia with high fat diet were administered with Shrimp paste powder, Shrimp ethanol extract, and Shrimp ethanol extract residues in serum to determine total lipid, phospholipid, triglyceride, total cholesterol, HDL cholesterol The effects of hyperlipidemia on atherosclerosis were also observed along with the Atherosclerosis Index (AI).

The levels of total lipid, phospholipid, triglyceride, LDL cholesterol, and VLDL cholesterol decreased with the administration of shrimp and ethanol extracts of shrimp, while the ratio of HDL-cholesterol was reduced by 14% in the hyperlipidemic group compared to the normal group. After the administration of shrimp powder and shrimp ethanol extract, the recovery pattern was confirmed.

Hyperlipidemia is an index of arteriosclerosis, which is an index of arteriosclerosis, in peripheral tissues due to the synthesis of triglycerides and secretion of chylomicron in the small intestine, the synthesis of triglycerides in the liver, the secretion of VLDL and LDL cholesterol, the synthesis of HDL cholesterol and the decrease of lipase activity. Due to the decrease in triglycerides, it was confirmed that shrimp ethanol extract as well as shrimp salt powder can reduce the risk of arteriosclerosis in high fat diet obese rats (see Tables 6 and 7).

Treatment Dose
(Mg / kg) Total lipid Phospholipid Triglyceride Mg / dl Normal 231.4 ± 50.6 ^e 116.4 ± 21.7 ^bcd 57.2 ± 8.54 ^c Control 331.7 ± 49.3 ^abc 146.7 ± 20.3 ^a 84.9 ± 7.16 ^a SR 200 286.5 ± 40.6 ^cde 119.7 ± 12.5 ^bcd 69.2 ± 3.47 ^b SRE 200 267.4 ± 37.8 ^de 115.2 ± 13.8 ^cd 63.2 ± 4.11 ^bc SRER 200 352.4 ± 41.5 ^ab 139.6 ± 14.4 ^abc 80.6 ± 7.21 ^a The assay procedure was described in the experimental methods. Values are mean ± S.D. for five experiments. Values followed by the same letter are not significantly different (p <0.05).

Treatment Dose
(Mg / kg) Cholesterol (mg / ㎗) AI Total HDL LDL VLDL Normal 61.4 ± 1.97 ^d 41.6 ± 1.43 ^a 9.49 ± 0.98 ^c 11.8 ± 0.87 ^c 0.48 ± 0.13 ^c Control 147.8 ± 11.5 ^a 35.6 ± 1.51 ^c 90.6 ± 8.25 ^a 16.7 ± 1.46 ^a 3.15 ± 0.76 ^a SR 200 95.6 ± 5.13 ^bc 39.5 ± 1.17 ^b 41.2 ± 6.08 ^b 14.1 ± 0.62 ^b 1.42 ± 0.51 ^b  SRE 200 91.1 ± 4.89 ^c 40.2 ± 1.01 ^ab 38.3 ± 7.11 ^b 13.3 ± 0.57 ^b 1.27 ± 0.39 ^b  SRER 200 139.5 ± 6.20 ^a 36.0 ± 1.33 ^c 85.2 ± 5.13 ^a 16.1 ± 1.25 ^a 2.88 ± 0.46 ^a The assay procedure was described in the experimental methods. Values are mean ± S.D. for five experiments. Values followed by the same letter are not significantly different (p <0.05).

2-4. Hepatic tissue and Feces  Triglycerides and cholesterol  Content change

Table 8 shows the effects of dietary hyperlipidemia-induced dietary hyperlipidemia on changes in lipid and cholesterol content in liver tissues when oral administration of Shrimp powder, Shrimp ethanol extract, and Shrimp ethanol extract residues is shown in Table 8. In the rats fed oral administration of dietary hyperlipidemia, shrimp salted ethanol extract, and shrimp salted ethanol extract residues, the cholesterol content of liver tissue was lower in all experimental groups compared to the control group. Showed no significant difference. The content of triglyceride was lower in both groups compared to the control group, but the shrimp ethanol extract residue group showed no significant difference, while the shrimp ethanol extract group was significantly decreased. This can be said that not only shrimp salt powder but also shrimp salt ethanol extract affects lipid metabolism of liver tissue, and indirectly proves that it is effective in diseases such as hyperlipidemia. Lipid content in feces decreased in both treatment groups, and fecal volume was also decreased. This resulted in the inhibition of fatty acid synthesis by increasing the concentration of adiponectin related to the breakdown of fat in the liver and muscle with the administration of ethanol extract of shrimp as well as shrimp.

Treatment Dose
(Mg / kg) Triglyceride Cholesterol Mg / g of tissue Normal 11.6 ± 0.89 ^d 3.52 ± 1.11 ^e Control 27.8 ± 4.13 ^ab 16.5 ± 2.18 ^a  SR 200 17.3 ± 2.81 ^c 10.9 ± 1.34 ^c SRE 200 15.4 ± 2.77 ^c 8.4 ± 0.72 ^d  SRER 200 23.9 ± 2.16 ^b 15.3 ± 0.96 ^a The assay procedure was described in the experimental methods. Values are mean ± S.D. for five experiments. Values followed by the same letter are not significantly different (p <0.05).

Treatment Dose
(Mg / kg) Fecal weight Cholesterol Triglyceride g / day Mg / day Normal 3.83 ± 1.16 ^a 1.49 ± 0.27 ^c 7.92 ± 0.97 ^f Control 4.47 ± 1.25 ^a 4.92 ± 0.93 ^a 13.6 ± 1.04 ^a  SR 200 4.40 ± 1.12 ^a 4.01 ± 0.61 ^ab 9.32 ± 0.78 ^de  SRE 200 4.45 ± 0.81 ^a 3.62 ± 0.74 ^b 8.97 ± 0.92 ^ef SRER 200 4.35 ± 0.92 ^a 4.77 ± 0.77 ^a 11.2 ± 1.12 ^b The assay procedure was described in the experimental methods. Values are mean ± S.D. for five experiments. Values followed by the same letter are not significantly different (p <0.05).

2-5. Effect on the production of lipid peroxide in the blood

After inducing dietary hyperlipidemia, the effects of Shrimp powder, Shrimp ethanol extract, and Shrimp ethanol extract residues on the lipid content, lipid peroxide production system and elimination system were observed (Table 10-11). The lipid peroxide content was 48.9 ± 2.49nmole / ml in the hyperlipidemia-induced experimental group, which was 2 times higher than the normal group's 26.4 ± 2.13nmole / ml, and the blood hydroxy radical content was increased more than 2 times. On the other hand, the experimental group administered with Shrimp powder, Shrimp ethanol extract, and Shrimp ethanol extract residue was found to have a statistically significant effect of reducing the hyperlipidemia, and the effect on superoxide dismutase (SOD) activity. In the hyperlipidemia-induced experimental group, the SOD enzyme activity was increased statistically significant, although it did not reach the normal group. As a result of this experiment, it was confirmed that the administration of shrimp ethanol extract as well as shrimp salt powder had the effect of enhancing the SOD activity.

Treatment Dose
(Mg / kg) Content MDA nmole / ml of serum Normal 26.4 ± 2.13 ^g Control 48.9 ± 2.49 ^a SR 200 34.2 ± 1.18 ^f SRE 200 32.5 ± 1.09 ^f SRER 200 41.8 ± 1.25 ^d The assay procedure was described in the experimental methods. Values are mean ± S.D. for five experiments. Values followed by the same letter are not significantly different (p <0.05).

Treatment Dose
(Mg / kg) Hydroxyl radical SOD Activity nmole / mg protein U / g protein Normal 2.63 ± 0.42 ^c 3.49 ± 0.73 ^a Control 5.42 ± 0.56 ^a 1.98 ± 0.19 ^c  SR 200 3.77 ± 0.35 ^b 2.77 ± 0.14 ^b SRE 200 3.46 ± 0.47 ^b 2.92 ± 0.18 ^b SRER 200 4.98 ± 0.38 ^a 2.07 ± 0.13 ^c The assay procedure was described in the experimental methods. Values are mean ± SD for five experiments. Values followed by the same letter are not significantly different (p <0.05).
SOD 1 Unit: Defined as the amount of enzyme that inhibits the rate of adrenochrome formation to 50%

Hereinafter, the formulation examples of the composition of the present invention will be described, but the present invention is not intended to limit the present invention but merely to explain in detail.

Formulation example  One. Powder  Produce

SRE 20 mg

Lactose 100 mg

Talc 10 mg

The above components are mixed and filled in airtight bags to prepare powders.

Formulation example  2. Preparation of tablets

SRER 10 mg

Corn starch 100 mg

Lactose 100 mg

2 mg magnesium stearate

After mixing the above components, tablets are prepared by tableting according to a conventional method for preparing tablets.

Formulation example  3. Preparation of capsules

SRE 10 mg

3 mg of crystalline cellulose

Lactose 14.8 mg

Magnesium Stearate 0.2 mg

The above components are mixed according to a conventional capsule preparation method and filled in gelatin capsules to prepare capsules.

Formulation example  4. Preparation of injections

SRE 10 mL

180 mg mannitol

Sterile sterilized water for injection 2974 mg

Na2HPO4,12H2O 26 mg

(2 ml) per 1 ampoule according to the usual injection preparation method.

Formulation example  5. Liquid  Produce

SRER 20 mL

10 g of isomerized sugar

5 g of mannitol

Purified water

Each component was added to purified water in accordance with the usual liquid preparation method and dissolved, and the lemon flavor was added in an appropriate amount. Then, the above components were mixed, and purified water was added thereto. The whole was adjusted to 100 ml with purified water, And sterilized to prepare a liquid preparation.

Formulation example  6. Manufacture of health food

SR-D 1000 mL

Vitamin mixture proper amount

70 [mu] g of vitamin A acetate

Vitamin E 1.0 mg

0.13 mg vitamin B1

0.15 mg of vitamin B2

0.5 mg vitamin B6

0.2 [mu] g vitamin B12

10 mg vitamin C

Biotin 10 μg

Nicotinic acid amide 1.7 mg

50 ㎍ of folic acid

Calcium pantothenate 0.5 mg

Mineral mixture quantity

1.75 mg of ferrous sulfate

0.82 mg of zinc oxide

Magnesium carbonate 25.3 mg

15 mg of potassium phosphate monobasic

Secondary calcium phosphate 55 mg

Potassium citrate 90 mg

100 mg of calcium carbonate

Magnesium chloride 24.8 mg

Although the composition ratio of the above-mentioned vitamin and mineral mixtures is mixed with a component suitable for a health food in a preferred embodiment, the compounding ratio may be arbitrarily modified. The granules may be prepared and used for preparing a health food composition according to a conventional method.

Formulation example  7. Manufacture of health drinks

SRE 1000 mL

Citric acid 1000 mg

100 g of oligosaccharide

Plum concentrate 2 g

Taurine 1 g

Purified water was added to a total of 900 ml

The above components were mixed according to a conventional health drink manufacturing method, and the mixture was heated at 85 DEG C for about 1 hour with stirring, and the solution thus prepared was filtered to obtain a sterilized 2-liter container, which was sealed and sterilized, &Lt; / RTI &gt;

Although the composition ratio is a composition that is relatively suitable for the preferred beverage in a preferred embodiment, the compounding ratio may be arbitrarily modified according to regional and ethnic preferences such as demand hierarchy, demand country, and usage.

Claims (7)

A pharmaceutical composition for the prevention and treatment of obesity or hyperlipidemia and atherosclerotic vascular disease, comprising shrimp salt powder, shrimp salt soluble solvent extract or polar solvent insoluble extract residue as an active ingredient. The method of claim 1,
The shrimp chopped powder is characterized in that the product is usually distributed in the form or dry powder thereof. The method of claim 1,
The soluble polar salt soluble extract of the salted shrimp is a composition soluble in a solvent selected from water containing purified water of shrimp powder, a lower alcohol having 1 to 4 carbon atoms or a mixed solvent thereof. The method of claim 1,
The shrimp salt polar solvent insoluble extraction residue is a composition characterized in that the residue is insoluble in a solvent selected from water containing purified water of shrimp powder, a lower alcohol having 1 to 4 carbon atoms or a mixed solvent thereof. The method of claim 1,
The hyperlipidemia and atherosclerotic vascular diseases are hyperlipidemia, arteriosclerosis, heart failure, hypertensive heart disease, arrhythmia, congenital heart disease, myocardial infarction, angina pectoris, stroke or peripheral vascular disease. Health functional food for the prevention and improvement of obesity or hyperlipidemia and atherosclerotic vascular disease, comprising shrimp salt powder, shrimp salt soluble solvent extract or polar solvent insoluble extract residue as an active ingredient. The method according to claim 6,
The dietary supplement is a dietary supplement that is a powder, granules, tablets, capsules or beverages.