JP2009280501A - Visceral fat accumulation inhibitor - Google Patents

Abstract

<P>PROBLEM TO BE SOLVED: To provide a safe and effective visceral fat accumulation inhibitor which is an ingredient originated from a natural substance and can be taken in a daily life to expect an effect. <P>SOLUTION: Provided is the visceral fat accumulation inhibitor containing L-arabinose and sucrose as active ingredients. The visceral fat accumulation inhibitor is obtained, for example, by adding, mixing and reacting 2 Kg of beat pulp with 2 L of an aqueous solution of arabanase at 55°C for 24 hours, squeezing the reaction product, passing 1.8 L of the obtained liquid through an ultrafiltration membrane (fractionation mol.wt.: 6,000), sequentially passing the filtrate through a cation exchange column (Diaion SK series), an anion exchange column (Diaion WA series) and a mixed bed column (Diaion SK series+PA series), adding sucrose, and then drying the mixture. <P>COPYRIGHT: (C)2010,JPO&INPIT

Description

  The present invention relates to a visceral fat accumulation inhibitor, a metabolic syndrome improving agent containing the visceral fat accumulation inhibitor, and a food for improving metabolic syndrome.

  Increasing cardiovascular disease due to overnutrition and lack of exercise has become a problem not only in the West, but also in Asia. Conventionally, preventive measures for arteriosclerotic diseases including myocardial infarction and cerebral infarction have been focused on measures against hypercholesterolemia, and other risk factors have been individually dealt with. However, on the basis of obesity and lack of exercise in recent years, there are very many cases where multiple risk factors are accumulated in one person based on obesity, and the onset of arteriosclerosis is also seen in many cases from such multiple risk factor syndromes. (Non-Patent Document 1).

  This multiple risk factor syndrome was called by various concepts such as syndrome X, death quartet, insulin resistance syndrome, visceral fat syndrome, etc. Also defined diagnostic criteria for metabolic syndrome. According to the standard, it corresponds to the accumulation of visceral fat (waist circumference is 85 cm or more for men, 90 cm or more for women), and (1) lipids (neutral fat in blood is 150 mg / dL or more or HDL cholesterol is Less than 40 mg / dL), (2) Abdominal blood glucose (100 mg / dL or more) and (3) Blood pressure (systolic blood pressure 130 mmHg or more or diastolic blood pressure 85 mmHg or more) from (1) to (3) to two or more If applicable, it is diagnosed as metabolic syndrome (Non-patent Document 1).

  Drug therapy for metabolic syndrome is not yet well established, and prescriptions for anti-obesity drugs are being investigated. However, mazindol is known as an anti-obesity drug that is approved for medical insurance in Japan, but the drug is accompanied by restrictions on use of BMI 35 or more and an insurance application period of 3 months or less. In addition, when drug treatment is individually performed for each risk factor of metabolic syndrome, there is a concern that the interaction with the drug combination may adversely affect the symptoms.For example, thiazide diuretics used as antihypertensive drugs are insulin sensitive It is known to adversely affect the reduced sugar / lipid metabolism (Non-patent Documents 2 and 3).

  On the other hand, L-arabinose is a non-caloric saccharide having a taste similar to sugar and showing poor absorbability. In nature, it exists as a constituent sugar of polysaccharides such as arabinan, arabinoxylan or arabinogalactan in hemicellulose of higher plants. In the simple sugar state, it is a saccharide with a rich dietary experience that is contained in fermented foods such as miso and sake, instant coffee, and the like, although in trace amounts. In addition, since it inhibits a disaccharide hydrolase such as sugar, an effect of suppressing an increase in blood sugar level when sugar or the like is ingested is also known. A body fat accumulation inhibitor (Patent Documents 1 and 2), an obesity preventive agent (Patent Document 3), a food for diabetes (Patent Document 4), and adiponectin containing L-arabinose by utilizing such characteristics of L-arabinose A secretagogue (Patent Document 5), an insulin resistance improving agent (Patent Document 5), an anti-arteriosclerosis agent (Patent Document 5) and the like are known. However, the effect of L-arabinose alone on visceral fat accumulation was not strong.

In addition, sucrose (sugar) is decomposed and absorbed into glucose and fructose by the sugar-degrading enzyme sucrase originally localized in the small intestinal mucosa. In the present invention, sucrose taken at the same time as L-arabinose is not degraded by the sucrose inhibitory activity of L-arabinose, and about 40% is not absorbed from the small intestinal mucosa and moves to the lower intestinal tract. It is known that sucrose that has not been absorbed and moved to the lower intestinal tract acts on the intestinal bacterial flora and, like various oligosaccharides, is known to have a bifidobacteria growth promoting action (Patent Document 6), but improves the intestinal environment. It was not clear how this would affect.
“Obesity / Metabolic Syndrome Medical Guidance”, Medical View, 2005, pp. 10-11 “Obesity / Metabolic Syndrome Medical Guidance”, Medical View, 2005, pp. 205-206 "Medical Syndrome Medical Guidance", Medical View, 2005, pp. 207-209 JP-A-7-309765 JP-A-7-242551 Japanese Patent Publication No. 6-812057 JP 2002-136272 A JP 2007-246443 A JP 2004-1113068 A

  An object of the present invention is to provide a safe and effective visceral fat accumulation inhibitor, a metabolic syndrome improving agent, and a metabolic syndrome-improving food, which are components derived from natural products and can be expected to have an effect by ingestion in daily life. To do.

  As a result of intensive studies in order to achieve the above-mentioned problems, the present inventors have found that by taking L-arabinose and sucrose at the same time, a good visceral fat accumulation inhibitory effect is exhibited. It came to.

  That is, the first of the present invention is a gist of a visceral fat accumulation inhibitor characterized by comprising L-arabinose and sucrose as active ingredients, and preferably L-arabinose is arabinan, arabinoxylan or Derived from an enzyme-treated product obtained by allowing an enzyme having an activity of liberating L-arabinose by acting on arabinan, arabinoxylan or arabinogalactan on a natural fiber-derived dietary fiber material containing arabinogalactan More preferably, L-arabinose contains 1 to 10% by mass with respect to sucrose.

  The second aspect of the present invention is a metabolic syndrome improving agent characterized by containing the visceral fat accumulation inhibitor described above.

  The third aspect of the present invention is to provide a food for improving metabolic syndrome characterized by containing the visceral fat accumulation inhibitor described above.

  According to the present invention, it is possible to provide a safe and effective visceral fat accumulation inhibitor, a metabolic syndrome improving agent, and a metabolic syndrome-improving food that are components derived from natural products and that can be expected to have an effect of ingestion in daily life. , Its intake is extremely useful for safely and effectively promoting the improvement of lifestyle-related diseases such as diabetes associated with visceral fat accumulation, arteriosclerosis, etc., that is, metabolic syndrome, which has become a problem in recent years It becomes.

  Hereinafter, the present invention will be described in detail.

  L-arabinose used as an active ingredient in the first aspect of the present invention is not particularly limited, and is commercially available, or hemicellulose such as arabinan, arabinoxylan or arabinogalactan contained in corn fiber, gum arabic, beet pulp and the like. Can be used that is produced by alkaline extraction and enzymatic decomposition or acid decomposition. Among these, it is preferable to use the method for producing L-arabinose, the L-arabinose-containing enzyme-treated product and the method for producing the same that were previously developed by the present inventors (for details, see JP-A-2001-286294). That is, it is a method of liberating L-arabinose by directly treating a natural fiber-derived dietary fiber material containing arabinan, arabinoxylan or arabinogalactin with an arabinan, arabinoxylan or arabinogalatan degrading enzyme.

  This method will be further described.

  Natural products containing arabinan, arabinoxylan or arabinogalactan include orange fiber, tangerine juice lees, apple fiber, apple juice lees, beet fiber, beet pulp, groundnut ginger, rice bran, corn fiber, corn cob, corn lees or soybean lees Among them, beet pulp, orange fiber, and apple fiber are preferable because of a large amount of L-arabinose released by enzyme treatment.

  Examples of the enzyme to be acted on include arabinan degrading enzymes such as arabinase (arabanase) and arabinofuranosidase. The origin of the arabinan-degrading enzyme includes bacteria (Bacillus Subtilis, Streptomyces sp.), Yeast (Rhodotorula sp.), Filamentous fungi (Aspergillus niger, A. oryzae, A. , Trichoderma reesei, T. viride, Trichosporon penicillatum, Rhizopus sp.), Etc., and the enzyme derived from Aspergillus is preferable because of its reactivity with the natural product. In particular, an enzyme derived from Aspergillus niger is more preferable.

  In addition to the above, commercially available hemicellulase enzyme agents such as cellulase, xylanase, pectinase, and galactanase can also be used as long as they have an activity of releasing L-arabinose from the natural product. Furthermore, it is also possible to improve the liberation amount of L-arabinose by combining two or more kinds of enzymes having different activities.

  As conditions for releasing L-arabinose, 0.5 to 50 times the amount of water containing 0.4 to 4000 units of enzyme is added to the raw material with respect to 100 g of the natural product as the raw material, and 20 to 90 ° C. The treatment may be performed while standing or stirring for 3 to 48 hours under the conditions of pH 2 to 9. In this case, 1 unit of enzyme is an amount of enzyme having an activity of releasing 1 micromole of L-arabinose per minute from linear arabinan.

  A highly purified product of L-arabinose can be purified from the enzyme-treated product thus obtained by a commonly used method. Specific examples include extraction from enzyme-treated products, removal of polysaccharide components by ultrafiltration, decolorization by activated carbon, desalting by ion exchange column chromatography, crystallization using a difference in solubility due to temperature difference, etc. The purification of L-arabinose used in the invention is not limited to these methods. Regarding crystallization, it is preferable to use the L-arabinose-containing crystalline powder sugar composition and the method for producing the same that were previously developed by the present inventors (for details, see JP-A No. 2004-261039).

  The purity of L-arabinose used in the present invention is not particularly limited, and a natural fiber-derived dietary fiber material containing arabinan, arabinoxylan or arabinogalactin is allowed to directly act on arabinan, arabinoxylan or arabinogalatan degrading enzyme. Even if the obtained enzyme-treated product is used as it is, or even if it is high-purity L-arabinose that has been subjected to purification steps such as extraction, decolorization, desalting, and crystallization from this enzyme-treated product, It may be an intermediate (for example, an extract, a decolorizing solution, a desalting solution, or a crystallization filtrate). Furthermore, it may be a mixture of such an enzyme-treated product, intermediate or high-purity product.

  The visceral fat accumulation inhibitor of the present invention may contain an effective amount of the above-mentioned L-arabinose or enzyme-treated product and sucrose, and the content can be appropriately set in consideration of the intake amount described later. .

  As the form of the visceral fat accumulation inhibitor of the present invention, a liquid or a liquid product encapsulated in a soft capsule, a powder prepared by adding various excipients as described above, granules, a tablet, a powder, Any form such as a capsule in which granules are further encapsulated may be used.

  When preparing a liquid product, it is concentrated to a solution of various concentrations as necessary, or as it is, or a surfactant, oil, alcohol, emulsifier, pH adjuster, preservative, antioxidant, thickener. 1 type, 2 types or more, such as a pigment | dye and a fragrance | flavor, can be mixed suitably as needed. The liquid product thus prepared may be enclosed in a soft capsule.

  In addition to L-arabinose and sucrose as active ingredients, in order to obtain powders, granules and tablets, extenders such as lactose, dextrose, cellulose, corn starch and potato starch, silica, talc, stearic acid, stearin Lubricants such as magnesium acid, calcium stearate and polyethylene glycol, binders such as starch, gum arabic, gelatin, methylcellulose, carboxymethylcellulose and polyvinylpyrrolidine, disintegrants such as starch, alginic acid, alginates and sodium starch glycolate, foaming Powders, granules, and tablets can be formed using a wetting agent such as an agent, pigment, sweetener, lecithin, polysorbate, or lauryl sulfate.

  Furthermore, the visceral fat accumulation inhibitor of the present invention may take a form in which various dietary fibers are blended. Dietary fiber may be water-soluble or insoluble, such as dextrin, indigestible dextrin, mannan, galactomannan, etc., water-soluble, crystalline cellulose, starch, etc. It is also possible to take the form of granules, tablets, soft drinks, carbonated drinks and the like. For example, as water-soluble dietary fibers, indigestible dextrins such as “Fiber Sol 2” and “Pine Fiber” manufactured by Matsutani Chemical Industry, and galactomannans such as “Sun Fiber” manufactured by Taiyo Kagaku are highly water-soluble. As dietary fiber mix | blended with the visceral fat accumulation inhibitor of this invention, it is especially preferable.

  The amount of intake of the visceral fat accumulation inhibitor of the present invention is not particularly limited, but is preferably 1 g to 30 g, more preferably 5 g to 15 g per day in terms of the amount of sucrose. In that case, as L-arabinose, it is preferable that it is 1-10 mass% with respect to sucrose, ie, 10 mg-3 g, and it is more preferable that it is 50 mg-1.5 g. Due to the sucrose inhibitory activity of L-arabinose, about 40% of sucrose is decomposed and transferred to the lower intestinal tract without being absorbed, but the inhibition of sucrose by L-arabinose is almost fully exerted by adding about 3% to sucrose. This is because the effect is no longer increased even if it is added more than 10%. In addition, the maximum no action amount of sucrose and L-arabinose is 5 g / Kg or more in the limit test, and there is no problem with the actual intake.

  Moreover, the visceral fat accumulation inhibitor of the present invention contains sucrose, which is a natural sweetener, as a main component, and contains 1 to 10% by mass of L-arabinose, which is similar in taste to sucrose and is also derived from natural products. Therefore, it can be used as an alternative to ordinary sweeteners (sugar). Since it can be used in the same manner as ordinary sweeteners, it is possible to avoid problems such as the taste does not match like artificial sweeteners, and the sweetness is too strong to control sweetness.

  The action of the visceral fat accumulation inhibitor of the present invention is presumed to originate primarily from the α-glucosidase inhibitory activity of L-arabinose. The mechanism of action of α-glucosidase inhibition of L-arabinose will be described in detail. According to a report by Susumu Tsukuda (J. Appl. Glucosci., 46 (1999)), L-arabinose is found in the duodenum and small intestinal mucosa. It inhibits disaccharide-degrading enzymes such as maltase and sucrase localized on the microvillous membrane surface (mucosal brush border) in an antagonistic manner. As a result, since the ingested carbohydrate is slowly decomposed into glucose and fructose, absorption in the duodenum and upper jejunum is reduced, and digestion and absorption are performed in the middle and lower part of the small intestine. This action suppresses intake of calories derived from carbohydrates, promotes burning of accumulated fat to suppress intake of calories, suppresses fat cell hypertrophy, etc. Is.

  Moreover, the visceral fat accumulation inhibitor of the present invention is also presumed as a second effect of sucrose whose decomposition and absorption are inhibited by the inhibition of L-arabinose by α-glucosidase. Sucrose, whose decomposition and absorption are inhibited, moves to the lower intestinal tract and is assimilated by intestinal bacteria to promote the synthesis of various short-chain fatty acids (acetic acid, propionic acid, butyric acid, etc.). These short chain fatty acids are absorbed in the cecum to the large intestine and used in the living body to promote lipid metabolism in the liver. Due to this action, like L-arabinose, the burning of accumulated fat is promoted, and fat cell hypertrophy is suppressed, and as a result, it has visceral fat accumulation inhibiting activity.

  On the other hand, it changes the intestinal microflora, and in addition to the already known growth-promoting effect on bifidobacteria, it shows the growth-promoting action on lactobacilli and the growth-inhibiting action of staphylococci, one of the bad bacteria. The effect of improving bowel environment by improving the intestinal environment (defecation frequency, amount of defecation, increase in stool water content, decrease in stool pH) is also related to the effect of the visceral fat accumulation inhibitor of the present invention.

  The second and third metabolic syndrome improving agents and the food for improving metabolic syndrome of the present invention contain the first visceral fat accumulation inhibitor of the present invention, and the form thereof is not particularly limited. Various additives, specifically surfactants, oils, alcohols, emulsifiers, pH adjusters, antiseptics, as long as the visceral fat accumulation inhibitor is used as it is and does not interfere with the metabolic syndrome improving action of the present invention. One or two or more of agents, antioxidants, thickeners, pigments, fragrances, and the like may be appropriately blended as necessary. Moreover, what is necessary is just to set content of a visceral fat accumulation | storage inhibitor suitably considering the intake amount mentioned above.

  Furthermore, it is also possible to mix with other natural products containing components having other visceral fat accumulation suppressing action, adipocyte differentiation inducing action, adiponectin secretion promoting action and the like. Such products include capsicin-containing capsicum, pepper, salmon, mustard, etc., sulfur-containing compounds such as leek, onion, garlic, leek, rakkyo, etc., caffeine-containing coffee, tea, green tea, cinnamon, Examples include various natural products including catechin, docosahexaenoic acid, eicosapentaenoic acid, branched chain amino acids, L-carnitine, anserine, carnosine, plant sterol, and the like, and powders and processed products thereof.

  EXAMPLES Hereinafter, although an Example demonstrates this invention in detail, this invention is not limited to this. In addition, L-arabinose and sucrose were quantified by high performance liquid chromatography (column; Aminex HPX-87P (manufactured by Bio-Rad), column temperature: 60 ° C., mobile phase: ion-exchanged water, flow rate 0.6 mL / min, detection. ; Differential refractive index).

Example 1 [Production 1 of visceral fat accumulation inhibitor]
To 200 g of apple pulp (manufactured by Nichiro), 200 mL of an aqueous solution of 2% by mass of Sumiteam ARS (manufactured by Shin Nippon Chemical Co., Ltd., arabanase titer 400 units / mL) was added, mixed, and reacted at 55 ° C. for 24 hours. The reaction product was vacuum-dried (40 ° C., 48 hours) to obtain 195 g of an enzyme-treated product. This enzyme-treated product contained 14.1 g of L-arabinose (purity in solid content; 7.4% by mass). This enzyme-treated product is pulverized with a ball mill, 140 g of sucrose (powdered sugar) and water are added, and then the granulated visceral fat accumulation inhibitor (L-arabinose 13. 8 g, containing 139 g of sucrose).

Example 2 [Production of visceral fat accumulation inhibitor 2]
To 200 g of mandarin orange pulp (produced by Ehime Prefectural Agricultural Cooperative), 400 mL of an aqueous solution of 2% by mass of Sumiteam PX (manufactured by Shin Nippon Chemical Co., Ltd., arabanase titer 100 units / mL) was added, mixed, and reacted at 55 ° C. for 24 hours. The reaction product was squeezed and 250 g of sucrose (granulated sugar) was added to obtain 500 mL of a liquid type visceral fat accumulation inhibitor (containing 17.8 g of L-arabinose and 250 g of sucrose).

Example 3 [Production of visceral fat accumulation inhibitor 3]
2 L of an aqueous solution of 2% by weight of Sumiteam PX (manufactured by Shin Nippon Chemical Co., Ltd., arabanase titer 100 units / mL) was added to 2 kg of beet pulp (manufactured by Hokkaido Sugar Industry), mixed, and reacted at 55 ° C. for 24 hours. The reaction product was squeezed, and 1.8 L of the juice was passed through an ultrafiltration membrane (fraction molecular weight: 6000) to obtain 4 L of a membrane permeate. This is sequentially passed through a cation exchange column (Diaion SK series), an anion exchange column (Diaion WA series), and a mixed bed column (Diaion SK series + PA series), and the desalted solution is concentrated on a rotary evaporator. As a result, 1 L of concentrated liquid was obtained. To this, 5 kg of sucrose (granulated sugar) and 5 kg of indigestible dextrin (made by Matsutani Chemical Industry, Pine Fiber) were added and diluted to 100 L with water. The diluted solution was applied to a spray-drying apparatus to evaporate water to obtain 10 kg of white to light yellow powder type visceral fat accumulation inhibitor (containing 220 g of L-arabinose and 4.5 kg of sucrose).

Example 4 [Production of visceral fat accumulation inhibitor 4]
2 L of an aqueous solution of 2% by weight of Sumiteam PX (manufactured by Shin Nippon Chemical Co., Ltd., arabanase titer 100 units / mL) was added to 2 kg of beet pulp (manufactured by Hokkaido Sugar Industry), mixed, and reacted at 55 ° C. for 24 hours. The reaction product was squeezed, and 1.8 L of the juice was passed through an ultrafiltration membrane (fraction molecular weight: 6000) to obtain 4 L of a membrane permeate. This is passed through a cation exchange column (Mitsubishi Chemical, Diaion SK series), anion exchange column (Same, Diaion WA series), and mixed bed column (Same, Diaion SK series + PA series) for desalting. The treatment liquid was concentrated with a rotary evaporator to obtain a concentrated liquid having a solid content of 70% by mass. The concentrated solution was gradually cooled to 10 ° C. for crystallization. The precipitated crystals were separated by a centrifugal filtration device, and white powder was obtained through vacuum drying and pulverization steps. To this, 1.8 kg of sucrose (powder sugar) was added to obtain 2 kg of a powder type visceral fat accumulation inhibitor (containing 170 g of L-arabinose and 1.8 kg of sucrose).

Example 5 [Production 1 of metabolic syndrome improving agent]
Using a rotary automatic soft capsule filling machine, 700 μL of a liquid type visceral fat accumulation inhibitor obtained in the same manner as in Example 2 was enclosed in 10 mm × 7 mm soft capsules mainly composed of gelatin. A metabolic syndrome improving agent (containing 25 mg of L-arabinose and 350 mg of sucrose per grain) was used.

Example 6 [Production 2 of metabolic syndrome improving agent]
A powder type visceral fat accumulation inhibitor obtained in the same manner as in Example 4, 10 parts by weight of lactose, 50 parts by weight of lactose and 40 parts by weight of corn starch were uniformly mixed. A tablet-type metabolic syndrome improving agent (containing 4.5 mg of L-arabinose and 45 mg of sucrose per tablet) was used.

Example 7 [Production of food for improving metabolic syndrome, coffee drink]
1.8 kg of roasted coffee beans were crushed and extracted with hot water at 95 ° C. to obtain 18 L of coffee extract. To this extract, 556 g of the visceral fat accumulation inhibitor obtained in Example 4 was added and dissolved well, and then cooled to room temperature to remove solids of 300 mesh or more. Further, sodium bicarbonate was added to adjust the pH to 6.0, and then an instantaneous sterilization treatment at 121 ° C. for 60 seconds was performed. After cooling, it was filled into a 300 mL capacity PET bottle to obtain a metabolic syndrome-improved coffee beverage (containing 470 mg of L-arabinose and 5 g of sucrose per bottle).

Example 8 [Production of food for improving metabolic syndrome, jelly beverage]
280 g of grapefruit concentrated fruit juice was added with 240 g of the visceral fat accumulation inhibitor obtained in Example 4, 40 g of γ-polyglutamic acid, 8 g of citric acid, 8 g of galactomannan, 6 g of agar, 4 g of fragrance, 2 g of trisodium citrate and 4212 g of water. After mixing and dissolving, 200 g each was filled into a tear pack container and sterilized at 90 ° C. for 30 minutes to obtain a metabolic syndrome-improving jelly beverage containing a tear pack (containing 0.9 g of L-arabinose and 10 g of sucrose per pack).

Test Example 1 [Confirmation of Visceral Fat Accumulation Activity 1 Animal Test]
SD male rats (manufactured by CLEA Japan, 4 weeks old) are high-fat and high-shoes containing 16% oil (Benibana oil 50: rapeseed oil 45: sesame oil 5), 8% lard and 26% sucrose. A group fed with a sugar diet (group C), a group fed with a feed containing 26% by mass of the visceral fat accumulation inhibitor obtained in Example 4 instead of sucrose (group A10, L-arabinose was about sucrose 10% by mass), a group fed with a feed containing 8% by mass of the visceral fat accumulation inhibitor obtained in Example 4 instead of sucrose, and 18% by mass of sucrose (Group A3, L-arabinose is sucrose About 3% by mass) and reared for 10 weeks. Body weight and waist circumference were measured every week during the breeding period. Fresh feces were collected at the end of the breeding period and the intestinal flora was observed. In addition, after the test period, epididymal fat, mesenteric fat, and perirenal fat (post-peritoneal fat) were removed as visceral fat, and the wet weight was compared. Moreover, the short chain fatty acid content in the cecal contents was compared.

  The results are shown in FIGS. As can be seen from FIGS. 1 and 2, suppression of weight gain and suppression of increase in waist circumference are observed, and from FIG. 3, it is clear that these effects are due to suppression of visceral fat accumulation. In addition, as shown in FIG. 4, the intestinal environment is changed by the action of L-arabinose and sucrose in the visceral fat accumulation inhibitor, and the short-chain fatty acid content is increased, thereby promoting the burning of accumulated fat and suppressing visceral fat accumulation. It is suggested that the effect of is stronger. Furthermore, it can be inferred from Table 1 that the change in the content of short-chain fatty acids is due to the change in the intestinal flora.

Test Example 2 [Confirmation of Visceral Fat Accumulation Activity 2 Human Test]
Twelve men who have a habit of drinking sweetened canned coffee (male, 12, 25-48 years old, BMI 20.1-26.2, body fat percentage 18.0-29.0%) are divided into 2 groups, Black coffee (P group) containing 5 g of sucrose as a placebo drink on one side, and coffee drink (T group) containing 5 g of the visceral fat accumulation inhibitor obtained in Example 7 on the other side. 3 cans per day for 3 months. Before and after the test, body weight and abdominal circumference were measured, and body fat percentage was measured by the impedance method.

  The physical measurement results are shown in Table 2. As is clear from Table 2, the T group ingested with the visceral fat accumulation inhibitor of the present invention for 3 months showed a decrease in both body weight and abdominal circumference as compared with the P group, and the body fat percentage decreased significantly. Indicated.

The result of having observed the change (when the test start time is set to 100) of the rat which ingested the feed containing a visceral fat accumulation inhibitor for 10 weeks is shown. The result of having observed the change of the waist circumference (when the test start time is set to 100) of the rat which ingested the feed containing a visceral fat accumulation inhibitor for 10 weeks is shown. The result of having compared the visceral fat wet weight (ratio (%) to a body weight) of the rat ingested the feed containing a visceral fat accumulation inhibitor for 10 weeks is shown. The result of having compared the short chain fatty acid content in the cecum contents of the rat which ingested the feed containing a visceral fat accumulation inhibitor for 10 weeks is shown.

Claims (5)

A visceral fat accumulation inhibitor comprising L-arabinose and sucrose as active ingredients. L-arabinose is obtained by allowing an enzyme having an activity of liberating L-arabinose by acting on arabinan, arabinoxylan or arabinogalatan to a dietary fiber material derived from a natural product containing arabinan, arabinoxylan or arabinogalactan The visceral fat accumulation inhibitor according to claim 1, wherein the visceral fat accumulation inhibitor is derived from the obtained enzyme-treated product. L-arabinose contains 1-10 mass% with respect to sucrose, The visceral fat accumulation | storage inhibitor of Claim 1 or 2 characterized by the above-mentioned. A metabolic syndrome improving agent comprising the visceral fat accumulation inhibitor according to any one of claims 1 to 3. A food for improving metabolic syndrome, comprising the visceral fat accumulation inhibitor according to any one of claims 1 to 3.