KR20040017891A - Dietary composition including levan for prevention and treatment of obesity - Google Patents

Abstract

PURPOSE: Provided is a dietary composition for prevention and treatment of obesity using levan or levan oligosaccharide. The dietary composition inhibits the formation and accumulation of body fat and increases UCP expression in adipose tissue. CONSTITUTION: A dietary composition for prevention and treatment of obesity is characterized by containing levan or levan oligosaccharide as an active ingredient, wherein solid levan is contained in the amount of 0.1-20 wt.% and liquid levan is contained in the amount of 0.1-8 wt.%. The composition is applied to dietary foods, medicaments and the like for improving obesity.

Description

Dietary composition including levan for prevention and treatment of obesity

The present invention relates to an obesity-enhancing dietary composition using levan, and more particularly, leban or levan oligosaccharides are involved in energy metabolism (breathing) of mammals, resulting in de-respiratory respiration to mitochondrial lining caused by decomposed protein (UCP). Levan can be used as a dietary food and medicine to treat obesity caused by daily diet by improving the proton leakage and the effect of improving obesity (reduction of visceral fat and peritoneal fat) It relates to a diet for improving obesity.

Obesity is the most serious nutritional problem in industrialized countries, and the incidence of obesity has recently increased significantly in our country. The cause of obesity is not yet clear, but body fat accumulation due to the imbalance between energy intake and consumption is known as the main cause [Grundy, Am. J. Clin. Nutr. 67 (suppl): s563-s572, 1998], combined factors such as fat intake and genetic factors have been shown to cause obesity [Albu et al., Nutr. Rev. 55: 150-156, 1997. Obesity is increasing not only in humans but also in pets. The severity of obesity has been closely related to various adult diseases (arteriosclerosis, diabetes, high blood pressure, etc.), which is a problem. Obesity is a condition in which the body has an excess of fat, which is caused by an excess intake of carbohydrates or fats supplied in the diet. The cause of obesity caused by excessive intake of sugar is not yet clear, but the sugars contained in food are digested to become monosaccharides, absorbed into the body through the small intestine, and the blood sugar rises to secrete insulin from its stimulation. It acts on the monosaccharides in the blood to be accepted by the fat cells accumulate in fat. Surplus energy in the living body is primarily accumulated as visceral fat (particularly, intestinal fat), and this visceral fat is easily accumulated and rapidly decomposed and consumed as compared to fat in other parts (particularly, subcutaneous fat). This visceral fat is considered to be a multi-risk factor for lifestyle disease (adult disease), which secretes fatty acids from white adipose tissue (WAT) in white fat cells directly into the liver via the portal vein, leading to insulin resistance. It enhances liposynthesis, resulting in diabetes, hypertension, and hyperlipidemia, which eventually become an important cause for the atherosclerosis to develop. In humans, obesity is known to be caused by the combined effects of genetic and environmental factors, but the main mechanism of occurrence is an imbalance between energy intake and consumption. When energy efficiency is poor, obesity occurs due to fat accumulation. More than one-third of body weight changes can be explained by genetic predisposition [Albu et al., Nutr. Rev. 55: 150-156, 1997. Recently, studies on the molecular predisposition of genetic predisposition to obesity have been carried out, and mutations of leptin, laptin receptor and carboxypeptidase E genes that cause obesity have been found in rodents. Homologs of these genes have been found in humans. Leptin is a hormone that regulates appetite and energy expenditure produced by the ob gene. It is secreted by white adipose tissue and regulates the appetite and satiety center by regulating the expression of the neuropeptide Y in the hypothalamus of the brain. It inhibits accumulation and weight gain. The tissues involved in energy consumption through exothermic reaction in adipose tissue are brown adipose tissue (BAT), and the uncoupling protein (UCP) present in the inner membrane of the brown adipose tissue mitochondria is adaptive heat generation ( is involved in adaptive thermogenesis. UCP prevents protons generated by oxidative phosphorylation in cell membranes from being used for ATP synthesis in the mitochondria and is used to produce heat, causing exothermic reactions and increasing energy expenditure, which contributes to weight control. Deconjugated protein-1 (UCP-1), which is mainly present in brown adipose tissue, exists as a protein of molecular weight 32 KD consisting of about 300 amino acids. UCP-1 has a structure consisting of repeating a domain consisting of about 100 amino acids three times, there is a membrane penetrating site forming a total of six channels, two in each domain. Thus, UCP-1 expresses the function of releasing heat by acting as a transporter for transporting protons. UCP-2 has 59% homology with UCP-1 and is widely expressed in systemic tissues such as lung, pancreas, heart, liver, brain, kidney, testis, WAT, BAT, skeletal muscle [Fleury C. et al., Nature Genet. 269-272, 1997; Gimeno R. et al., Diabetes, 900-906, 1997], along with UCP-3, which is found primarily in muscles, has been recognized to regulate energy metabolism [Matsuda J. et al. FEBS Lett. 418: 200-204, 1997; Boss O. et al. FEBS Lett. 408: 39-42, 1997. In relation to these genes, studies have shown that nutritional factors regulate the expression of leptin and UCP genes [Rippe C. et al., Am. J. Physiol. Endocrinol. Metab. 279: 293-300, 2000; Watson P. Am. J. Physiol. Endocrinol. Metab. 279: 356-365, 2000] Studies are underway on substances with anti-obesity effects by increasing UCP gene expression [Oi Y. et al., J. Nutr. 129: 336-342, 1999; Cha S. et al., J. Nutr. 131: 2636-2642, 2001.

Prior to the present invention, the inventors have produced a novel microsaccharide-derived fructose polymer called Levann with high purity of 99% or higher (Korean Patent Publication Nos. 176410 and 145946).

General characteristics of the fructose polymer Levan are as follows.

Fructose polymers are known as levan and inulin, and they are composed differently in the method of binding fructose residues. Inulin is composed of beta-2,1 bonds and is a storage carbohydrate having a relatively small molecular weight of 20-60 in the degree of polymerization (DP). It is contained in a large amount of pork, chicory, and dahlia. In contrast, Levan is a water-soluble fructose polymer represented by Glu- (Fru) n, where Glu represents a glucose residue, Fru represents a fructose residue, and n represents a number of about 10 ⁵ . It is made from sugar by the fructose transfer reaction of levanschkrase. A number of methods for preparing levans using levanschkrase have been reported. For example, US Pat. No. 4,879,228 and International Patent Publication No. 86-4091 disclose leban from sugar using microorganisms that act in metabolic processes. In the present invention, the present inventors have proposed a recombinant levansch that is largely expressed in E. coli transformed using the Levanschkrase gene of Zymomonas mobilis and Pseudomonas aurantiaca S-4380. Levan was produced using Kraje [Korean Patent Publication Nos. 176410 and 145946; And Korean Patent Application No. 2001-41532.

Studies on the physiological effects of inulin on weight loss and hyperlipidemia have been reported [Delzenne N. et al., Nutr. Metab. Cardiovasc. Dis. 11: 118-121, 2001; Mortensen A. et al. Nutr. Res. 22: 473-480, 2002], there are no studies of obesity and patents by levan or levan oligosaccharides.

Therefore, the present inventors conducted the above study to develop the expression inhibitory factor of the obesity gene, and when the diet consisting of the natural polysaccharides levane, suppressing the formation and accumulation of body fat, increase the expression of UCP in adipose tissue The present invention was completed by finding the fact and confirming the anti-obesity effect by Levan.

Accordingly, it is an object of the present invention to provide a diet for improving obesity containing levane or levane oligosaccharides.

In addition, the present invention is another object to provide a diet foods and pharmaceuticals consisting of the composition.

1 is a (A) brown adipose tissue, (B) skeletal muscle of rats administered for 6 weeks using a diet containing powdered Levan in rats grown on a normal diet and obese mice induced by a high fat diet. C) mRNA expression level of deconjugated protein (UCP) in white adipose tissue is shown.

The present invention is characterized by an obesity-enhancing dietary composition containing Levan or Levan oligosaccharides.

In addition, diet foods and pharmaceuticals made of the composition is another feature.

The present invention will be described in more detail as follows.

Levan is a safe biopolymer produced by various food microorganisms and plants, including enteric lactic acid bacteria, and efficiently reaches the large intestine and is used as an energy source by the intestinal microorganisms. Levan produces only fructose and very small amounts of glucose upon complete degradation by acid hydrolysis or heat treatment, so there are very few side effects expected in animals that have ingested levan. In addition, Levan is partially decomposed in the small intestine of the animal is used as a calorie source, but most Levan reaches the intestine and fermented by the intestinal lactic acid bacteria can be expected to reduce the calorie absorbed compared to the same weight of monosaccharides.

The anti-obesity and therapeutic effects of Levan are confirmed both when the Levan is administered in a powder state such as powder state or pellet form or in a liquid dissolved in water. Lebanese concentration of the liquid can be expected to prevent and improve the obesity at 0.1 to 8% by weight, preferably 7% by weight. In the case of liquid phase, there is a slight increase in viscosity at a concentration of 6% by weight, but there is no big problem in intake. If it is less than 0.1% by weight, the effect of the addition of levane may be reduced. If it exceeds 8% by weight, mixing with low water content becomes difficult. It is preferable to use 0.1 to 20% by weight of the solid levan. If it is less than 0.1% by weight, the effect of the levane addition may be reduced, and if it exceeds 20% by weight, the palatability is inferior.

In the case of solid Levan, no significant side effects such as diarrhea and bleeding were observed in the rats at 10% by weight.

Levan was supplied as a liquid oral and powdered diet to observe the effects of dietary Levan on changes in energy metabolism such as body fat formation, leptin and UCP gene expression in rats.

Levan oligosaccharide is a substance synthesized by heat treatment, acid hydrolysis or enzymatic method of levan. It is an oligosaccharide whose chemical structure is the same as that of levan and is reduced in size. Therefore, levan oligosaccharide also has the effect of preventing and improving obesity proposed in the present invention. The foods to be prepared include all kinds of foods such as solid foods, creamy or jam-like semi-flowing foods, gel foods, beverages, etc., which are in the form of capsules, granules, tablets, drinks, etc. Beverages (soft drinks, juices, coffee, tea, milk, barley tea, lactic acid bacteria beverages), confectionery (sweets, bread, chewing gum, chocolate, ice cream, pudding, water yolk) and the like. As mentioned above, the levan or levan oligosaccharides are water-soluble and have no difficulty in mixing even when mixed with other solutions, and maintain homogeneity, thus exhibiting the same effect of obesity as solids.

In addition to levane or levane oligosaccharides, pharmaceutically acceptable carriers or excipients may be used in the form of tablets, powders, granules, capsules, suspensions, emulsions or parenteral or multi-dose formulations for parenteral administration.

The effective dose of the active ingredient represented by the active fraction may vary depending on the age, physical condition, weight, etc. of the patient, but is generally administered within the range of 1 to 100 mg / kg (weight) per day. In addition, the dose is administered once a day or divided several times a day within the effective dosage range per day.

Hereinafter, the present invention will be described in more detail based on the following examples, but the present invention is not limited thereto.

Reference Example

(1) Preparation of Sample

Levans were prepared in the laboratory of the inventors using Jimonas mobilelis (Korean Patent Publication Nos. 176410 and 145946).

(2) Levan Assay

The Levan solution was filtered through a 0.45 μm filter membrane, and then 20 μl of the filtrate was injected into HPLC [System Gold, Beckman Corporation] to quantify the Levan content. HPLC analysis conditions were detected by the refractive index (refractive index) of the sugar concentration while flowing distilled water at a rate of 0.4 ml per minute using a column maintained at 50 ℃ (Ionpak KS-802, Shodex). Levante was composed of more than 99.9% fructose and traces of glucose, with a molecular weight of more than one million.

(3) Breeding and diet of experimental animals

Three-week-old Sprague-Dawley male rats were used for 1 week, followed by feeding a high-fat diet for 4 weeks to 6 weeks. A diet containing 0% by weight, 3% by weight, and 5% by weight of the Levan powder, respectively, was administered for 10 to 6 weeks after the induction of obesity. The normal control group was fed AIN-76A diet # 100000 [Dytes, USA] during the 12-week experimental period from 4 weeks of age, and the high-fat diet group used bee tallow as a fat source to feed AIN-76A high-fat diet # 100496 [Dytes Inc., USA] was fed to feed 40% of the total calories to fat [Table 1]. Each experimental group was six.

division Normal diet High-fat diet Casein 200 200 Methionine 3 3 Corn starch 150 150 Sucrose 500 345 cellulose 50 50 Corn oil 50 - Uji - 205 Mixed inorganic 35 35 Mixed Vitamin 10 10 Choline Bitartate 2 2 Fat content% (of total calories) 11.7 40.0

Experimental animals were separated and bred one by one, and water and diet were supplied without restriction. Dietary intake and body weight were measured twice a week during the experiment. The dietary efficiency (FER) was calculated by dividing the weight gain during the experiment period by the dietary intake during the experiment period from the experimental diet supply day to the sacrifice day.

(4) Sample Collection and Analysis

1) Sample Collection

Experimental animals were sacrificed at 16 weeks of age to collect blood and organs. Interscapular brown adipose tissue, epididymal fat, visceral fat, peritoneal fat, and soleus muscle were separated and weighed, and immediately frozen with liquid nitrogen. It was. Blood was collected by sacrificial heart puncture and centrifuged at 3000 rpm for 15 minutes to obtain serum, and these samples were stored at -70 ° C until analysis.

2) fat cell size measurement

The size of fat cells was measured by digesting visceral adipose tissue extracted from 16-week-old experimental animals. Adipose tissue was digested with NaCl-buffer containing collagenase at 37 ° C. for 1 hour and filtered to obtain fat cells, and the size of the fat cells was observed under a scaled microscope. The average value was obtained by measuring the diameter of 30 cells for each tissue.

3) Blood Lipid Analysis

The total cholesterol, HDL cholesterol, and triglyceride contents of the serum were measured using a kit of Sigma Chemical.

4) Blood Leptin and Insulin Content Analysis

Serum leptin content was measured by using the Linco leptin assay Kit (Linco, USA) to measure the radioimmunity, and insulin content by rat insulin standards (Linco) Was measured.

5) Decomposed protein mRNA analysis

Reverse transcriptase and PCR were used to measure the expression level of the de-conjugated protein. The expression levels of UCP-1, UCP-2 and UCP-3 mRNA were measured in brown adipose tissue, a major tissue for exothermic reactions, and UCP-2 mRNA in epididymal adipose tissue for analysis of white adipose tissue, a major tissue for fat accumulation and metabolism. Expression levels were measured and UCP-2 and UCP-3 mRNA contents were measured in the hind limb muscles to determine the UCP mRNA content of the muscles that occupy most of the body composition.

RNA was isolated and quantified from tissues isolated from laboratory animals. For the synthesis of cDNA from the isolated total RNA, 2 μg of RNA was heat-treated at 70 ° C. for 5 minutes and then left at 4 ° C. for 5 minutes, and M-MLV [Promega, Product No. M1705] 200 U, dNTP ( each 2.5 mM) mix 2 μl of RNasin [Promega, product No. N2111] 40 U, 1 μl of oligo (dT) primer [Promega, product No. C1101], adjust 25 μl with DEPC-water, and adjust to 42 ℃ 1 CDNA was synthesize | combined under the conditions for 30 hours and 75 degreeC.

Primers were prepared to measure the expression level of UCP from the synthesized cDNA, and β-actin was used as a comparative gene. The primers used in the experiment and the obtained DNA size are as follows.

UCP-1 5'-primer: 5'-TAC CCA CAT CAG GCA ACA G-3 '(SEQ ID NO: 1)

3'-primer: 5'-TCA TTG CAC AGC TGG GTA C-3 ', (SEQ ID NO: 2)

DNA size obtained: 842 bp

UCP-2 5'-primer: 5 -ACA GCA GCC TGT ATT GCA G-3 '(SEQ ID NO: 3)

3'-primer: 5'-TTG TAG GCT TCG ACA GTG C-3 ', (SEQ ID NO: 4)

DNA size obtained: 428 bp

UCP-3 5'-primer: 5'-ACC ATG GTT GGA CTT CAG C-3 '(SEQ ID NO: 5)

3'-primer: 5'-AGT TCC CAG CGT ATC CAT G-3 '(SEQ ID NO: 6)

DNA size obtained: 450 bp

PCR conditions for measuring the expression level of the gene is as follows.

Tag polymerase [TaKaRa Co., Ltd.] 0.125 μl, 10 × PCR buffer 2.5 μl, dNTP mix 2 μl, 25 μl with distilled water, 94 ℃ 3 minutes, 94 ℃ 30 seconds, 60 ℃ 1 minute, 72 ℃ After repeating 1 minute 30 seconds, 30 times, PCR was performed once at 94 ° C. 30 seconds, 60 ° C. 1 minute, 72 ° C. 10 minutes, and once. PCR products were separated by electrophoresis at 100 V using 1.5% agarose gel, and then bands were detected at absorbance 304 nm. The expression of the gene was confirmed by the shade of the band on the photograph.

5. Processing of data

One-way ANOVA was used to test the differences between the diets and Duncan's multiple range test was performed at α = 0.05. Significance was tested at α = 0.05 and α = 0.01 levels, and all statistical analyzes were processed using SAS program. Results are expressed as mean ± standard deviation (SD).

Example 1: Dietary Intake, Weight Gain and Dietary Efficiency

Table 2 shows the changes in dietary intake, weight gain and dietary efficiency of rats administered for 6 weeks using a diet containing powdered Jimonas levan in rats grown on a normal diet and obese rats fed with a high-fat diet. Indicated. There was no difference in dietary intake between groups, and weight gain and dietary efficiency were higher in the high-fat diet group than in the normal control group, but the effects of the Levan diet group did not show statistical significance. There was a significant difference between the groups without the (p <0.05)].

division Feed Intake (g / day) Weight gain (g / day) Dietary efficiency Normal control 21.10 ± 3.18 1.33 ± 0.80 0.059 ± 0.034 High fat control 25.13 ± 3.07 2.74 ± 0.46 0.109 ± 0.011 5% Leban 26.35 ± 3.76 2.45 ± 0.83 0.094 ± 0.022 3% Leban 24.09 ± 3.87 2.39 ± 1.36 0.096 ± 0.053 P-value 0.1531 0.1446 0.1713

Example 2 Weight of Adipose Tissue

The results of comparing the brown fat tissue, epididymal fat, visceral fat, and peritoneal fat weight according to dietary fat and levan supply are shown in Table 3 below, and each adipose tissue was expressed in terms of tissue weight for unit weight. The weight of brown adipose tissue was increased in the rats fed the high fat diet than the rats fed the normal diet, and this increase was decreased by the Levan diet. The epididymal fat weight tended to increase with high fat diet, but there was no statistical significance. Visceral fat weight, which was more than doubled by the high-fat diet, was reduced by the Leban diet, and this effect was greater in the 5% Leban group than in the 3% Leban group. Peritoneal fat weight was higher in the high fat control group (2.78 ± 0.25g / 100g body weight) than in the normal control group (1.28 ± 0.51g / 100g body weight) and was less than the high fat control group in the 5% Levan group (2.07 ± 0.55g / 100g body weight). The results showed that the increase in visceral and peritoneal fat of rats fed a Levan-containing diet decreased compared to rats fed only a high-fat diet, indicating that dietary Levan inhibited body fat accumulation. There is a significant difference between groups that do not have a common sign (p <0.05)].

division Brown adipose tissue (mg organ / 100 g body weight) Epididymal tissue (mg organ / 100 g body weight) Visceral fat (mg organ / 100 g body weight) Peritoneal Fat (mg organ / 100 g body weight) Normal control 0.89 ± 0.42 ^c 1.66 ± 0.61 1.79 ± 0.81 ^b 1.28 ± 0.51 ^b High fat control 1.51 ± 0.49 ^a 2.10 ± 0.44 3.68 ± 1.12 ^a 2.78 ± 0.25 ^a 5% Leban 1.42 ± 0.19 ^ab 2.24 ± 0.69 2.79 ± 0.71 ^ab 2.07 ± 0.55 ^ab 3% Leban 1.01 ± 0.32 ^bc 2.27 ± 0.73 3.52 ± 0.71 ^bc 2.20 ± 0.46 ^a P-value 0.0329 0.4370 0.0102 0.0039

Example 3: Size of Fat Cells

When fat cells were separated and measured in visceral adipose tissue, they showed similar results to body fat reduction by Levan-containing diet, and the increase in fat cell size increased by high-fat diet was shown in Table 4 below. There is a significant difference between groups that do not have a common sign in a group (p <0.05)].

division Fat cell size (um) Normal control 74.8 ± 14.1 ^c High fat control 120.3 ± 28.4 ^a 5% Leban 98.0 ± 6.7 ^b 3% Leban 100.2 ± 16.8 ^b P-value 0.0324

Example 4: Blood Lipid Content

Serum total cholesterol was not different among the experimental groups, but HDL cholesterol was lower in the high fat control group than the normal control group, and the Leban diet group was significantly increased than the high fat control group [Table 5]. Serum triglycerides (triglycerides) were significantly increased in the high-fat control group at 139.62 ± 106.32 mg / dL compared to 78.49 ± 11.84 mg / dL in the normal control group, while significantly decreased in the levane fed group at 60.50 ± 9.82 mg / dL, 54.26 ± 10.81 mg / dL, which is less than the 50% level of the high fat control group, was lower than the normal control group. The Leban diet after high fat diet did not affect the total cholesterol in blood, but increased HDL cholesterol, and the triglyceride in blood was significantly decreased by the Leban supply, which was more decreased than the normal diet. This shows that Levan has an excellent effect on improving blood lipids (there are significant differences between groups that do not have a common sign in the same group) (p <0.05).

division Plasma total cholesterol (mg / dl) Plasma HDL Cholesterol (mg / dl) Plasma Triglycerides (mg / dl) Normal control 78.33 ± 20.35 58.82 ± 7.42 ^a 78.49 ± 11.84 ^ab High fat control 72.53 ± 7.51 42.86 ± 3.90 ^b 139.62 ± 106.32 ^a 5% Leban 76.51 ± 15.28 51.50 ± 10.94 ^ab 60.50 ± 9.82 ^b 3% Leban 72.97 ± 15.91 52.59 ± 10.05 ^ab 54.26 ± 10.81 ^b P-value 0.9092 0.0647 0.0557

Example 5: Leptin and Insulin Content in Blood

The blood leptin content was significantly lower in the 5% Leban group compared to the high fat control group, and the 50% level (5.24 ± 2.84 ng / ml) of the high fat control group (10.53 ± 1.82 ng / ml) by the 5% Leban diet. Decreased to nearly normal control levels [Table 6]. Blood insulin content was also decreased by the Levan diet, which was lower in the 3% Leban group than the high fat control group, and the 5% Leban group was reduced to the normal control level. As a result of this study, Leban supply decreased blood insulin, indicating that Levan regulates the secretion of insulin, a hormone that is involved in lipid and energy metabolism. In addition, visceral fat accumulation is associated with an increase in insulin resistance. The Leban diet showed a decrease in visceral fat along with a decrease in visceral fat. Blood leptin, like blood insulin, was also reduced in rats fed Levan's diet. Leptin production varies with body fat production and is positively correlated with body fat percentage and fat cell growth. . Therefore, the decrease of leptin in blood was found to be due to the reduction of body fat accumulation and suppression of insulin in blood by Leban diet. Leptin acts as an inhibitory mechanism for obesity, and when energy is accumulated excessively, leptin production increases, which can be used as an indicator of obesity. (There was a significant difference between the groups with no common sign in the same figure (p <0.05)).

division Leptin (ng / ml) Insulin (ng / ml) Normal control 3.74 ± 0.62 ^b 1.55 ± 0.56 ^b High fat control 10.53 ± 1.82 ^a 2.74 ± 0.77 ^a 5% Leban 5.24 ± 2.84 ^b 1.60 ± 0.60 ^b 3% Leban 8.40 ± 2.31 ^a 2.30 ± 0.62 ^ab P-value 0.0004 0.1652

Example 6: UCP mRNA Expression

The results of UCP expression of brown adipose tissue, white adipose tissue, and hind limb muscles isolated from experimental animals using RT-PCR are shown in FIG. 1. The expression of UCP-1, UCP-2, and UCP-3 in brown adipose tissue can be seen to be induced by a high fat diet, which was further induced by the Levan-containing diet. In addition, this expression increase was more pronounced in the 5% Levan group than in the 3% Leban group. UCP-2 and UCP-3 of the hind limb muscle were measured to determine the expression level of UCP-2 in skeletal muscle. . The UCP-2 mRNA content of epididymal fat tended to increase slightly in the Levan diet group, but there was no significant difference. The expression of UCP-3, which is specifically expressed in skeletal muscle, increased in rats fed 5% Levan, indicating that Levan intake could contribute significantly to increased energy consumption.

Example 7: Preparation of Tablets

Levan 88 g

5 g of Ca (whey)

0.7 g of Fe

0.04 g of vitamin D3 (100.00 IU / g)

0.09 g of vitamin B1

0.09 g of vitamin B2

0.09 g of vitamin B6

2 g green tea extract

Excipient 3.99 g

Total amount 100 g

The tablets were prepared by direct tableting method after mixing the ingredients listed above finely. The total amount of each tablet is 300 mg, of which the active ingredient content is 264 mg.

Example 8: Preparation of Beverages

After dissolving 10 g of Levan of the present invention in an appropriate amount of water, an appropriate amount of glucose, reduced maltose, citric acid and sodium citrate was added thereto, and an aromatic substance was added thereto. After mixing the above mixture evenly well to make 100ml to prepare a beverage composition. The mixture was heated at 100 ° C. for 15 minutes and then stored in a cold place to produce a low calorie beverage. At this time, taurine, myo-inositol, folic acid, pantothenic acid, etc. may be added alone or together.

Example 9: Preparation of Bread

The composition of the baking dough is as follows. The blending ratio was formulated with each of the following ingredients based on 100% flour, and the leban was added so that the final concentration was 10% relative to the 60% water supply used for baking.

East 6%

8% sugar

Salt 1.8%

Margarine 8%

Starch Milk 4%

60% of water

The baking process was performed according to the direct kneading method. Baking dough was put in a baking mold and baked in an oven and cooled at room temperature.

Example 10 Toxicity Test

Levan (levan oligosaccharides) was dissolved in sterile distilled water and 100 mg / kg (150 mg / kg) each was orally administered to mice (10 mice per group) for 2 weeks. Observations were made for 14 days, no abnormalities were found, and no biochemical symptoms were observed in the blood.

As described above, the dietary composition containing levan or levan oligosaccharide according to the present invention suppresses body fat accumulation by reducing visceral fat weight, peritoneal fat weight, and fat cell size, and increases blood HDL cholesterol level to increase lipid metabolism. It improves and decreases blood leptin and insulin concentrations affects the formation of fat cells and body fat. In addition, by increasing the amount of UCP-3 mRNA expression of the muscle and UCP of brown adipose tissue provides an effect of improving obesity according to the effect of increasing the energy consumption in the body.

Claims (6)

An obesity-enhancing dietary composition comprising levan as an active ingredient. The diet of claim 1, wherein the levan comprises levan oligosaccharides. The diet of claim 1, wherein when the levan is solid, it contains 0.1 to 20% by weight. The diet of claim 1, wherein the levan is present in an amount of 0.1 to 8% by weight. A diet food comprising the composition of claims 1 to 4. An obesity prevention and treatment agent containing the composition of claims 1 to 4.