Promoter for production of hydrogen in intestines

Abstract

The present disclosure addresses the problem of providing a functional component that promotes the production of hydrogen in the intestine. Provided is an oligosaccharide comprising at least one cyclic sugar residue and at least one linear sugar residue, wherein the linear sugar is a sugar in which a formyl group in an aldose is converted to CO2X (wherein X represents a hydrogen atom or a counter cationic group for a carboxylic acid salt) or CH2OH. The oligosaccharide is useful as an active ingredient of a promoter for the production of hydrogen in the intestine.

Description

Intestinal hydrogen production promoter

[0001] The present disclosure relates to an agent for promoting intestinal hydrogen production.

[0002] For commercial purposes, the food industry classifies bacteria that are beneficial to human health, such as lactic acid bacteria and bifidobacteria, as good bacteria, and bacteria that cause opportunistic infections such as sepsis as bad bacteria. Good bacteria, such as lactic acid bacteria and bifidobacteria, digest dietary fiber to produce short-chain fatty acids, which induce regulatory T cells and maintain homeostasis in the intestinal tract.

[0003] Meanwhile, intestinal bacteria include not only lactic acid bacteria and bifidobacteria, which do not produce hydrogen, but also hydrogen-producing bacteria, which do (Non-Patent Document 1). Hydrogen has clinical benefits for many diseases, including neurological disorders, cardiovascular diseases, respiratory diseases, diabetes, liver diseases, and metabolic syndrome. To date, more than 1,000 papers have been published on the medical application of hydrogen, including more than 90 reports of human clinical trials (Non-Patent Document 1). For this reason, there is growing recognition that hydrogen-producing bacteria have superior health benefits compared to other beneficial bacteria, such as lactic acid bacteria and bifidobacteria, which cannot produce hydrogen.

[0004] It has been reported that lactulose produces significant amounts of hydrogen in the human large intestine (Non-Patent Document 2). It has also been reported that the portal vein hydrogen concentration required to obtain the expected antioxidant effect of hydrogen generated in the large intestine is 4-5 μmol / L (Non-Patent Document 3).

[0005] Medical Gas Research 2023 Jul-Sep; 13(3): 108-111.Digestive Diseases and Sciences 1994 Jul;39(7):1505-10.British Journal of Nutrition 2012 Feb;107(4):485-92.

[0006] Recently, with the increasing health consciousness of consumers, the use of foods containing various functional ingredients has expanded. For example, functional ingredients aimed at improving the intestinal environment generally include specific beneficial bacteria such as lactic acid bacteria and bifidobacteria, or ingredients that induce the products of these specific beneficial bacteria. On the other hand, although lactulose has been reported as a functional ingredient that promotes intestinal hydrogen production, considering the bioavailability of hydrogen generated in the intestine, functional ingredients with even better hydrogen production-promoting effects are desired.

[0007] The present disclosure aims to provide a functional ingredient that promotes intestinal hydrogen production.

[0008] As a result of extensive research, the present inventors have found that certain oligosaccharides have the effect of promoting intestinal hydrogen production. Furthermore, the present inventors have also found that these certain oligosaccharides have the effect of promoting intestinal short-chain fatty acid production. The present disclosure was completed through further research based on these findings.

[0009] That is, the present disclosure provides the following aspects of the invention. Item 1. An intestinal hydrogen production promoter comprising, as an active ingredient, an oligosaccharide consisting of one or more cyclic sugar residues and linear sugar residues, wherein the linear sugar is a sugar in which the formyl group of an aldose has been converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH. Item 2. The intestinal hydrogen production promoter according to Item 1, wherein the aldose is glucose. Item 3. The intestinal hydrogen production promoter according to Item 1 or 2, wherein the oligosaccharide is lactobionic acid and / or a salt thereof. Item 4. The intestinal hydrogen production promoter according to Item 1 or 2, wherein the oligosaccharide is lactitol. Item 5. The intestinal hydrogen production promoter according to any one of Items 1 to 4, which is in the form of a food or drink. Item 6. The intestinal hydrogen production promoter according to Item 5, further comprising lactic acid bacteria. Item 7. The intestinal hydrogen production promoter according to Item 5 or 6, wherein the active ingredient is 0.001% by weight or more. Item 8. An agent for promoting intestinal short-chain fatty acid production, comprising as an active ingredient an oligosaccharide consisting of one or more cyclic sugar residues and a linear sugar residue, wherein the linear sugar is a sugar in which the formyl group of an aldose is converted to COX (X represents hydrogen or a counter cation group of a carboxylate) or CHOH. Item 9. The agent for promoting intestinal short-chain fatty acid production according to Item 8, wherein the aldose is glucose. Item 10. The agent for promoting intestinal short-chain fatty acid production according to Item 8 or 9, wherein the oligosaccharide is lactobionic acid and / or a salt thereof. Item 11. The agent for promoting intestinal short-chain fatty acid production according to Item 8 or 9, wherein the oligosaccharide is lactitol. Item 12. The agent for promoting intestinal short-chain fatty acid production according to any one of Items 8 to 11, wherein the short-chain fatty acid is selected from the group consisting of formic acid, acetic acid, propionic acid, butyric acid, isobutyric acid, isovaleric acid, valeric acid, methylbutyric acid, and succinic acid. Item 13. Item 14. A method for promoting intestinal hydrogen production, comprising administering to a subject in need of promotion of intestinal hydrogen production an effective amount of an oligosaccharide consisting of one or more cyclic sugar residues and linear sugar residues, wherein the linear sugar is a sugar in which the formyl group of an aldose is converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH.Item 15. Use of an oligosaccharide consisting of one or more cyclic sugar residues and linear sugar residues for the manufacture of an agent for promoting intestinal hydrogen production, wherein the linear sugar is a sugar in which the formyl group of an aldose has been converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH. Item 16. An oligosaccharide consisting of one or more cyclic sugar residues and linear sugar residues for use in the treatment of a disease associated with intestinal hydrogen deficiency, wherein the linear sugar is a sugar in which the formyl group of an aldose has been converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH. Item 17. Non-therapeutic use of an oligosaccharide consisting of one or more cyclic sugar residues and linear sugar residues for promoting intestinal hydrogen production, wherein the linear sugar is a sugar in which the formyl group of an aldose has been converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH. Item 18. Item 18. A method for promoting intestinal short-chain fatty acid production, comprising administering an effective amount of an oligosaccharide consisting of one or more cyclic sugar residues and a linear sugar residue to a subject in need of promotion of intestinal short-chain fatty acid production, wherein the linear sugar is a sugar in which the formyl group of an aldose has been converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH. Item 19. Use of an oligosaccharide consisting of one or more cyclic sugar residues and a linear sugar residue for the manufacture of an agent for promoting intestinal short-chain fatty acid production, wherein the linear sugar is a sugar in which the formyl group of an aldose has been converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH. Item 20. An oligosaccharide comprising one or more cyclic sugar residues and linear sugar residues for use in treating a disease associated with a deficiency of short-chain fatty acids in the intestine, wherein the linear sugar is a sugar in which the formyl group of an aldose has been converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH. Item 21. A non-therapeutic use of an oligosaccharide comprising one or more cyclic sugar residues and linear sugar residues for promoting intestinal short-chain fatty acid production, wherein the linear sugar is a sugar in which the formyl group of an aldose has been converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH.

[0010] According to the present disclosure, a functional ingredient for promoting intestinal hydrogen is provided. Also according to the present disclosure, a functional ingredient for promoting intestinal short-chain fatty acid production is provided.

[0011] 1 shows the intestinal hydrogen production promoting effect of the intestinal hydrogen production promoter of the present disclosure.

[0012] 1. Intestinal Hydrogen Production Promoter The intestinal hydrogen production promoter of the present disclosure contains a specific oligosaccharide as an active ingredient. Note that, in the present disclosure, oligosaccharide refers to a polysaccharide having two or more sugar residues. Below, embodiments of the intestinal hydrogen production promoter of the present disclosure are described in detail.

[0013] 1-1. Active ingredient The specific oligosaccharide that serves as the active ingredient of the intestinal hydrogen production promoter of the present disclosure comprises one or more cyclic sugar residues (hereinafter also referred to as "cyclic sugar a") and chain sugar residues (hereinafter also referred to as "chain sugar b"), and the chain sugar b is a sugar in which the formyl group of an aldose has been converted to COX (X represents hydrogen or a counter cation group of a carboxylate) or CHOH.

[0014] The cyclic sugar a is not particularly limited, but typically includes pyranose, more preferably glucose, galactose, mannose, etc. The number of cyclic sugar a residues constituting a given oligosaccharide may be one or more, and is preferably 1 to 5, more preferably 1 to 4, even more preferably 1 to 3, and even more preferably 1 to 2.

[0015] Among the chain sugars b, sugars in which the formyl group of an aldose has been converted to COX (X represents hydrogen or a counter cation group of a carboxylate) include, for example, aldonic acid, uronic acid, aldaric acid, and salts thereof, preferably aldonic acid and salts thereof, more preferably gluconic acid, galactonic acid, mannonic acid, and salts thereof, and even more preferably gluconic acid and salts thereof. In the case of salts, X (counter cation group of a carboxylate) may be an alkali metal or alkaline earth metal, or an organic base, with alkali metals such as potassium and sodium, and alkaline earth metals such as calcium, and organic bases such as monoethanolamine, diethanolamine, triethanolamine, aminomethylpropanol, and aminomethylpropanediol.

[0016] Among the chain sugars b, the sugar in which the formyl group of an aldose is converted to CHOH is not particularly limited as long as it is an alditol, and preferred examples include sorbitol, xylitol, mannitol, galactitol, etc., and more preferred example is sorbitol.

[0017] In the present disclosure, the active ingredient can be any combination selected from the types and numbers of cyclic sugar a residues and the types of chain sugar b residues described above, and one type from the any combination may be used alone, or multiple types may be used in combination.

[0018] Preferred specific examples of the predetermined oligosaccharide include lactobionic acid or a salt thereof (cyclic sugar a is galactose, and chain sugar b is gluconic acid or a salt thereof), lactitol (cyclic sugar a is galactose, and chain sugar b is sorbitol), maltobionic acid (cyclic sugar a is glucose, and chain sugar b is gluconic acid), and oligosaccharides having a structure in which the cyclic sugar a of these oligosaccharides is repeated 2 to 3 times, and more preferred specific examples include lactobionic acid or a salt thereof, and lactitol.

[0019] The method for producing the predetermined oligosaccharide can be any known method without any particular limitation, including, for example, a method for producing the predetermined oligosaccharide by extracting the predetermined oligosaccharide present in a natural product, a method for producing the predetermined oligosaccharide by decomposing a natural polysaccharide into the predetermined oligosaccharide using an acid or a glycosidase, a method for producing the predetermined oligosaccharide by transferring a natural carbohydrate using a glycosyltransferase, a method for producing the predetermined oligosaccharide by converting a natural carbohydrate using a glycosylphosphorylase, and a method for producing the predetermined oligosaccharide by fermenting a sugar that serves as a substrate for the predetermined oligosaccharide with a microorganism capable of producing the predetermined oligosaccharide.

[0020] The content of the active ingredient contained in the intestinal hydrogen production promoter of the present disclosure can be determined appropriately depending on the method for producing the active ingredient, the formulation form, the product classification, and / or the intestinal hydrogen production promoting effect to be imparted.

[0021] For example, when the intestinal hydrogen production promoter of the present disclosure is a functional food material or pharmaceutical material, the content of the active ingredient may be, for example, 30% by weight or more, preferably 35% by weight or more, more preferably 40% by weight or more, and even more preferably 43% by weight or more, with the upper limit being, for example, 100% by weight or less, 90% by weight or less, 80% by weight or less, 70% by weight or less, 60% by weight or less, or 50% by weight or less. When the intestinal hydrogen production promoter of the present disclosure is a functional food material or pharmaceutical material, specific ranges of the content of the active ingredient include, for example, 30 to 100% by weight, 30 to 90% by weight, 30 to 80% by weight, preferably 35 to 70% by weight, more preferably 40 to 60% by weight, and even more preferably 43 to 50% by weight.

[0022] For example, when the intestinal hydrogen production promoter of the present disclosure is a food, beverage, or pharmaceutical product, the content of the active ingredient may be, for example, 0.001 wt% or more, preferably 0.01 wt% or more or 0.1 wt% or more, more preferably 0.5 wt% or more or 1 wt% or more, and even more preferably 2 wt% or more, 3 wt% or more, or 4 wt% or more, with the upper limit being, for example, 60 wt% or less, 50 wt% or less, 40 wt% or less, 30 wt% or less, 20 wt% or less, or 10 wt% or less. When the intestinal hydrogen production promoter of the present disclosure is a food, beverage, or pharmaceutical product, the specific range of the content of the active ingredient may be, for example, 0.001 to 60 wt%, preferably 0.01 to 60 wt% or 0.1 to 60 wt%, more preferably 0.5 to 50 wt% or 1 to 40 wt%, and even more preferably 2 to 30 wt%, 3 to 20 wt%, or 4 to 10 wt%.

[0023] 1-2. Other Components In addition to the active ingredient(s), the intestinal hydrogen production promoter of the present disclosure may or may not contain other nutritional components and / or other pharmacological components, as long as the effects of the present invention are not impaired. The other nutritional components and other pharmacological components that may be contained are not particularly limited as long as they are usable in foods, beverages, or oral pharmaceuticals, and include, for example, carbohydrates (oligosaccharides other than the active ingredient(s) and dietary fiber), fatty acids, minerals, vitamins, amino acids, peptides, microorganisms (lactic acid bacteria, bifidobacteria, butyric acid bacteria, etc.), etc. Furthermore, when the active ingredient is produced by fermentation using a microorganism, the other components may include medium components used to culture the microorganism and co-produced components of the microorganism. When the intestinal hydrogen production promoter of the present disclosure contains these other nutritional components and / or other pharmacological components, these other nutritional components and / or other pharmacological components may be used alone or in combination.

[0024] In addition to the active ingredients described above, the intestinal hydrogen production promoter of the present disclosure may or may not contain bases and / or additives, etc., as necessary to prepare the desired formulation. The bases and additives that may be included are not particularly limited as long as they are usable in foods, beverages, or oral medications, and include, for example, excipients, disintegrants, lubricants, binders, thickeners, monohydric lower alcohols (1 to 5 carbon atoms), solid oils, higher alcohols (6 or more carbon atoms, specifically 6 to 24, preferably 8 to 24 carbon atoms), water-soluble polymers, surfactants, polyhydric alcohols, pH adjusters, buffers, antioxidants, preservatives, chelating agents, water, etc. When the intestinal hydrogen production promoter of the present disclosure contains these bases and / or additives, these bases and / or additives may be used alone or in combination.

[0025] 1-3. Formulation Form and Product Classification The formulation form of the intestinal hydrogen production promoter of the present disclosure is not particularly limited and may be any of liquid, semi-solid (gel, paste), solid (granules, fine granules, powder, tablet, capsule), etc. Furthermore, the intestinal hydrogen production promoter of the present disclosure may be a non-emulsified formulation such as an aqueous formulation or an oil-based formulation, or an emulsified formulation such as an oil-in-water emulsion formulation or a water-in-oil emulsion formulation.

[0026] Furthermore, product categories of the intestinal hydrogen production promoter of the present disclosure include functional food materials, pharmaceutical materials, foods and beverages, and oral medicines.

[0027] Food and drink products are not particularly limited, but examples include fermented milk (drinkable yogurt, etc.), lactic acid bacteria drinks, dairy drinks (coffee milk, fruit milk, etc.), tea drinks (green tea, black tea, oolong tea, etc.), fruit and vegetable drinks (drinks containing fruit juices such as orange, apple, grape, etc., and vegetable juices such as tomato, carrot, etc.), alcoholic drinks (beer, happoshu, wine, etc.), carbonated drinks, soft drinks, water-based drinks, and other beverages; and processed foods such as fermented milk (set yogurt, soft yogurt, etc.), sweets, instant foods, and seasonings.

[0028] Foods and beverages also include functional foods. Functional foods refer to foods that have a certain functionality for the living body, and examples include health functional foods such as foods for specified health uses (including conditionally designated foods for specified health uses [FOSHU]) and foods with nutrient function claims, functional food, special-purpose foods, nutritional supplements, health supplements, supplements (for example, tablets, coated tablets, sugar-coated tablets, capsules, liquids, and other dosage forms), and beauty foods (for example, diet foods). Furthermore, functional foods may be special-purpose foods such as foods for the sick, powdered milk for pregnant and nursing women, infant formula, foods for the elderly, and foods for caregivers.

[0029] 1-4. Uses The intestinal hydrogen production promoter of the present disclosure is used to promote hydrogen production in the intestine. It has been reported that hydrogen produced in the intestine scavenges hydroxyl radicals in intestinal epithelial cells, protecting the intestinal wall from oxidative stress, and that excess hydrogen diffuses through the cell membrane, some of which circulates throughout the body via the bloodstream (Medical Gas Research 2023 Jul-Sep; 13(3): 108-111.). Therefore, the intestinal hydrogen production promoter of the present disclosure can be used to treat various diseases or conditions for which the preventive or therapeutic effects of hydrogen intake or administration have been reported (Journal of Japanese Biochemical Society 87(1): 82-90 (2015)).

[0030] Specifically, the intestinal hydrogen production promoter of the present disclosure can be used for the purpose of preventing or ameliorating the following diseases or conditions: Neurodegeneration (caused by dementia, Parkinson's disease, depression, anesthetic neurotoxicity, or carbon monoxide neurotoxicity) Metabolic syndrome (caused by diabetes, dyslipidemia, arteriosclerosis, obesity, or hypertension) Inflammation (caused by sepsis, rheumatoid arthritis, asthma, periodontal disease, wounds, or chronic inflammatory disorders) Side effects of anticancer drugs (caused by radiation therapy or chemotherapy) Ischemia-reperfusion injury (caused by cerebral infarction, myocardial infarction, organ transplant, cardiopulmonary resuscitation, glaucoma, etc.) Interstitial cystitis, detoxification Mitochondrial disease or myositis Lactic acid accumulation or easy fatigue Aging Hearing loss

[0031] 2. Intestinal Short-Chain Fatty Acid Production Promoter The intestinal short-chain fatty acid production promoter of the present disclosure contains a specific oligosaccharide as an active ingredient. The active ingredient, formulation, and product classification of the intestinal short-chain fatty acid production promoter of the present disclosure are the same as those described above in "1. Intestinal Hydrogen Production Promoter."

[0032] The intestinal short-chain fatty acid production promoter of the present disclosure is used for promoting intestinal short-chain fatty acid production. The short-chain fatty acid may be any fatty acid having less than 6 carbon atoms, specifically, formic acid, acetic acid, propionic acid, butyric acid, isobutyric acid, isovaleric acid, valeric acid, methylbutyric acid, and succinic acid, more preferably butyric acid and succinic acid. When the intestinal short-chain fatty acid production promoter of the present disclosure contains lactobionic acid and / or a salt thereof as an active ingredient, it is particularly preferably used for promoting intestinal butyric acid production.

[0033] The intestinal short-chain fatty acid production promoter of the present disclosure can be applied to various diseases or conditions for which the preventive or therapeutic effects of promoting intestinal short-chain fatty acid production have been reported.

[0034] Specifically, the intestinal short-chain fatty acid production promoter of the present disclosure can be used for purposes such as suppressing obesity, suppressing appetite, regulating the immune system, suppressing allergies, improving bowel movements, suppressing blood sugar level increases, preventing diabetes, promoting mineral absorption, and enhancing intestinal barrier function by promoting mucin secretion in the intestine.

[0035] Each feature disclosed herein may be combined with any other feature disclosed herein.

[0036] The present invention will be described in more detail below with reference to examples, but the configurations and combinations thereof in each embodiment are merely examples, and additions, omissions, substitutions, and other modifications of the configurations may be made as appropriate within the scope of the present invention. The present disclosure is not limited by the embodiments, but is limited only by the scope of the claims.

[0037] (1) Experimental Materials: Lactobionic acid (purity 98%, Fujifilm Wako Pure Chemical Industries, Ltd.), lactitol (LC-0, Bussan Food Science Co., Ltd.), lactulose (purity > 98%, Tokyo Chemical Industry Co., Ltd.), and lactose (lactose monohydrate, purity 99.5%, Daicel Corporation).

[0038] (2) Experimental Animals, Diet, and Rearing Thirty 5-week-old male Sprague-Dawley rats (Japan SLC) were used. The rats were housed in individual cages at a room temperature of 23±2°C, humidity of 50-70%, and a 12-hour light-dark cycle (light period 7:00-19:00). After delivery, the rats were reared on the control diet shown in Table 1 for 7 days to allow them to acclimate to the environment. The rats were divided into five groups based on body weight and net hydrogen (H2) excretion, and each group was fed the control, Examples 1 and 2, and Comparative Examples 1 and 2 diets shown in Table 1 for 14 days.

[0039]

[0040] (3) Measurement and Analysis (3-1) Net H2 excretion was measured 3, 7, and 10 days after the start of the study, and on the final day of the study. On the final day of the study, portal vein blood was collected under anesthesia with isoflurane inhalation.

[0041] (3-2) After collecting the portal vein blood, the small intestine (from the ligament of Treitz to the ileocecal valve) was immediately removed. After measuring the total length of the small intestine, a 15 cm section from 5 cm below the ligament of Treitz was collected as a jejunum sample, and a 15 cm section from 70 cm below the ligament of Treitz was collected as an ileum sample. The jejunal and ileal samples were incised longitudinally, washed with saline, and the mucosa was scraped off. The cecum was then removed, and the cecal contents were collected. DNA was extracted from bacteria in the cecal contents using a commercially available kit (ISOFECAL for Beads Beating, Nippon Gene). The pH, short-chain fatty acid concentration (HPLC method), and ammonia concentration (colorimetric method) of the cecal contents were also measured.

[0042] (3-3) Statistical analysis After checking the homogeneity of variance of the data, if the variances were homogeneous, significant differences were confirmed using one-way analysis of variance and analyzed using the Tukey-Kramer post-hoc test. If the variances were unequal, significant differences were confirmed using the Kruskal-Wallis test and analyzed using the Steel-Dwass test. The significance level was set at 5%.

[0043] (4) Results (4-1) The measurement results of (3-1) above are shown in Table 2, and the net hydrogen discharge amount and portal vein hydrogen concentration from the measurement results are shown in Figure 1.

[0044] There were no differences in food intake or weight gain between the groups (Table 2). Net H2 excretion in the three groups given lactose derivatives (Examples 1, 2, and Comparative Example 1) was significantly higher than that of the control group from day 3 onward. The increases in Examples 1 and 2 were similar and more pronounced than those in Comparative Example 1 (Table 2, Figure 1). The net H2 excretion in Examples 1 and 2 exceeded the portal vein hydrogen concentration (4-5 μmol / L) required to achieve the expected antioxidant effect of hydrogen generated in the large intestine, as reported in Non-Patent Document 3 (British Journal of Nutrition 2012 Feb;107(4):485-92). On the other hand, no increase in net H2 excretion was observed in Comparative Example 2. Portal vein H2 concentration also showed similar changes to net H2 excretion and the area under the curve (AUC) for net H2 excretion (Table 2).

[0045] (4-2) The results of the measurement in (3-2) above for the control, Examples 1 and 2, and Comparative Example 2 are shown in Table 3.

[0046]

[0047] The cecal tissue weight was significantly higher in Examples 1 and 2 compared to the control, but no significant increase was observed in Comparative Example 2. The cecal content weight was also significantly higher in Examples 1 and 2 compared to the control, with a significant increase observed in Example 2. Furthermore, like the cecal tissue weight, the cecal content weight in Comparative Example 2 was similar to that of the control.

[0048] The pH of the cecal contents was significantly lower in Examples 1 and 2 compared to the control and Comparative Example 2. The total amount of short-chain fatty acids in the cecal contents was higher in Examples 1 and 2 compared to the control and Comparative Example 2. Of the short-chain fatty acids, succinic acid and butyric acid were each significantly higher in Examples 1 and 2 compared to the control, with succinic acid in particular increasing significantly in Example 1.

Claims

1. An agent for promoting intestinal hydrogen production, comprising as an active ingredient an oligosaccharide consisting of one or more cyclic sugar residues and linear sugar residues, wherein the linear sugar is a sugar in which the formyl group of an aldose is converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH.

2. The intestinal hydrogen production promoter according to claim 1, wherein the aldose is glucose.

3. The intestinal hydrogen production promoter according to claim 1, wherein the oligosaccharide is lactobionic acid and / or a salt thereof.

4. The intestinal hydrogen production promoter according to claim 1, wherein the oligosaccharide is lactitol.

5. The intestinal hydrogen production promoter according to claim 1, which is a food or drink.

6. The intestinal hydrogen production promoter according to claim 5, further comprising lactic acid bacteria.

7. The intestinal hydrogen production promoter according to claim 5, containing 0.001% by weight or more of the active ingredient.

8. An agent for promoting intestinal short-chain fatty acid production, comprising as an active ingredient an oligosaccharide consisting of one or more cyclic sugar residues and linear sugar residues, wherein the linear sugar is a sugar in which the formyl group of an aldose is converted to CO2X (X represents hydrogen or a counter cation group of a carboxylate) or CH2OH.

9. The intestinal short-chain fatty acid production promoter according to claim 8, wherein the aldose is glucose.

10. The intestinal short-chain fatty acid production promoter according to claim 8, wherein the oligosaccharide is lactobionic acid and / or a salt thereof.

11. The intestinal short-chain fatty acid production promoter according to claim 8, wherein the oligosaccharide is lactitol.

12. The intestinal short-chain fatty acid production promoter according to claim 8, wherein the short-chain fatty acid is selected from the group consisting of formic acid, acetic acid, propionic acid, butyric acid, isobutyric acid, isovaleric acid, valeric acid, methylbutyric acid, and succinic acid.

13. The intestinal short-chain fatty acid production promoter according to claim 10, wherein the short-chain fatty acid is butyric acid.

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