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A series of safety assessments were performed on hydrogenated resistant maltodextrin prepared by converting the reducing terminal glucose of resistant maltodextrin into sorbitol. The reverse mutation assay did not show mutagenicity. Acute and 90-day subchronic oral toxicity studies in rats showed no death was observed in any groups, including the group receiving the highest single dose of 10 g/kg body weight or the highest dose of 5 g/kg body weight per day for 90 days. Mucous or watery stools were observed in the hydrogenated resistant maltodextrin treatment group on the acute study, which were transient and were associated with the osmotic pressure caused by intake of the high concentrations. Subchronic study showed dose-dependent increases in the weights of cecum alone, cecal contents alone, and cecum with cecal contents as well as hypertrophy of the cecal mucosal epithelium, which are considered to be common physiological responses after intake of indigestible carbohydrates. These results indicated that the no observed adverse effect level (NOAEL) of hydrogenated resistant maltodextrin was 10 g/kg body weight or more on the acute oral toxicity study and 5.0 g/kg body weight/day or more on the 90-day subchronic repeated oral toxicity study in rats. Further study performed in healthy adult humans showed that the acute no-effect level of hydrogenated resistant maltodextrin for diarrhea was 0.8 g/kg body weight for men and more than 1.0 g/kg body weight for women. The results of the current safety assessment studies suggest that hydrogenated resistant maltodextrin is safe for human consumption.

Background: It has been reported that low-viscous and fermentable dietary fiber and nondigestible oligosaccharides enhance mineral absorption. Resistant maltodextrin, nonviscous, fermentable and soluble source of dietary fiber, has several physiological functions. However, influence of resistant maltodextrin on mineral absorption is unclear. Aim of the study: We conducted balance studies in rats to investigate effects of resistant maltodextrin and hydrogenated resistant maltodextrin on apparent mineral absorption. Methods: In experiment 1 (Exp. 1), 40 rats were fed test diets based on AIN-93G with or without resistant maltodextrin or hydrogenated resistant maltodextrin for 2 weeks. In experiment 2 (Exp. 2), 32 rats were cecectomized (CX) or sham-operated (Sham) and fed diets with or without hydrogenated resistant maltodextrin for 1 week. Results: In Exp. 1, ingestion of resistant maltodextrin and hydrogenated resistant maltodextrin dose-dependently enhanced apparent absorption rates of Ca, Mg, Fe and Zn, and increased cecal fermentation with cecal expansion. In Exp. 2, the absorption rates of Ca and Mg were significantly enhanced by ingestion of hydrogenated resistant maltodextrin in Sham group but not in CX group. The promotion of Fe and Zn absorption was not affected by cecectomy. Conclusion: Ingestion of resistant maltodextrin and hydrogenated resistant maltodextrin increased apparent Ca and Mg absorptions dependent on cecal fermentation, while other mechanisms may also be involved in promotion of apparent Fe and Zn absorption by resistant maltodextrin.

In order to confirm the mechanism how postprandial elevation of triacylglycerol is suppressed by resistant maltodextrin (Fibersol-2), we conducted the following experiments. Firstly, Rats were fed a high-fat diet with resistant maltodextrin at 0% (control), 2.5% or 5% for 5 weeks to determine the lipid amount excreted in the feces of the last three days. The total lipid and triacylglycerol excreted in rat feces were significantly increased in a dose-dependent manner by the ingestion of resistant maltodextrin. Secondly, 10 healthy adult subjects were administrated a beverage containing 5 g resistant maltodextrin or placebo for 10 days, and crossed over after an 11-day washout. Total lipid excreted in feces was determined by collecting all the feces for the last three days. Fecal weight and fecal lipid amount of the subjects increased significantly with the ingestion of resistant maltodextrin compared to the placebo ingestion. Thirdly, oil emulsion prepared with resistant maltodextrin was assessed for its hydrolysis rate by lipase. The hydrolysis rate of lipid by lipase was not affected by resistant maltodextrin. Lastly, micelle emulsion was prepared with or without resistant maltodextrin, and their stability was compared. Resistant maltodextrin inhibited the decomposition of micelles and stabilized micellar structure. From these results, it was suggested that resistant maltodextrin suppresses lipid absorption and promotes the excretion of lipid into feces by delaying the release of fatty acids from micelles in the lipid absorption process. No inhibitory effect on lipase activity was observed by resistant maltodextrin.

還元難消化性デキストリンの食後血糖値に及ぼす影響を動物実験およびヒト試験において検討した。SD系雄性ラットを用い, 還元難消化性デキストリンを2.5-80%添加した糖負荷試験の結果, 5%添加で最も強い抑制効果がみられ, それ以上の添加においても同等の効果を示した。また, 健常成人男女9名を対象とし, 還元難消化性デキストリンを2.5-10g添加した食事負荷試験の結果, 5g以上の添加で有意な抑制効果が認められ, 用量依存性が認められた。次に健常成人男女10名を対象として還元難消化性デキストリンおよび難消化性デキストリンをそれぞれ5g添加した際の血糖上昇抑制効果を比較した結果, その効果はほぼ同等であることが確認された。これらの結果から, 還元難消化性デキストリンは食後血糖上昇抑制効果を有し, その効果の程度は難消化性デキストリンと同等であることが確認された。

Resistant maltodextrin (RM) is a novel soluble, nonviscous dietary fiber. Its metabolizable energy (ME) and net energy (NE) values derived from nutrient balance studies are unknown, as is the effect of RM on fecal microbiota. A randomized, placebo-controlled, double-blind crossover study was conducted (n = 14 men) to determine the ME and NE of RM and its influence on fecal excretion of macronutrients and microbiota. Participants were assigned to a sequence consisting of 3 treatment periods [24 d each: 0 g/d RM + 50 g/d maltodextrin and 2 amounts of dietary RM (25 g/d RM + 25 g of maltodextrin/d and 50 g/d RM + 0 g/d maltodextrin)] and were provided all the foods they were to consume to maintain their body weight. After an adaptation period, excreta were collected during a 7-d period. After the collection period, 24-h energy expenditure was measured. Fluorescence in situ hybridization, quantitative polymerase chain reaction, and 454 titanium technology-based 16S rRNA sequencing were used to analyze fecal microbiota composition. Fecal amounts of energy (544, 662, 737 kJ/d), nitrogen (1.5, 1.8, 2.1 g/d), RM (0.3, 0.6, 1.2 g/d), and total carbohydrate (11.1, 14.2, 16.2 g/d) increased with increasing dose (0, 25, 50 g) of RM (P < 0.0001). Fat excretion did not differ among treatments. The ME value of RM was 8.2 and 10.4 kJ/g, and the NE value of RM was -8.2 and 2.0 kJ/g for the 25 and 50 g/d RM doses, respectively. Both doses of RM increased fecal wet weight (118, 148, 161 g/d; P < 0.0001) and fecal dry weight (26.5, 32.0, 35.8 g/d; P < 0.0001) compared with the maltodextrin placebo. Total counts of fecal bacteria increased by 12% for the 25 g/d RM dose (P = 0.17) and 18% for the 50 g/d RM dose (P = 0.019). RM intake was associated with statistically significant increases (P < 0.001) in various operational taxonomic units matching closest to ruminococcus, eubacterium, lachnospiraceae, bacteroides, holdemania, and faecalibacterium, implicating RM in their growth in the gut. Our findings provide empirical data important for food labeling regulations related to the energy value of RM and suggest that RM increases fecal bulk by enhancing the excretion of nitrogen and carbohydrate and the growth of specific microbial populations.

The effect of methylcarbonylmethyl 2(S)-14-(4-guanidino-benzoyloxy) phenyl] propionate methanesulfonate (TT-S24) on experimental pancreatitis in rats was examined in comparison with that of camostat. TT-S24 showed a preventive effect on increases in plasma amylase activity and pancreatic weight induced by cerulein injection. TT-S24 also reduced an increase in plasma amylase activity induced by taurocholate. TT-S24 effectively prevented the mortality induced by an injection of a mixture of trypsin and taurocholate. TT-S24 showed no effect on an increase in amylase activity 6 h after duodenum ligation (closed duodenal loop pancreatitis), indicating that the drug had no effect on the initiation and propagation step of closed duodenal loop pancreatitis. On the other hand, TT-S24 reduced an increase in amylase activity 6 h after release of the duodenum ligation. TT-S24 showed anti-trypsin, anti-kallikrein, anti-thrombin and anti-plasmin activities. The effect of TT-S24 on some experimental pancreatitis models was nearly equal to or somewhat more potent in most instances to that of camostat. Therefore, TT-S24 should be useful in the clinical treatment of pancreatitis.

The intestinal microbiota compositions of 92 men living in Japan were identified following consumption of identical meals for 3 days. Fecal samples were analyzed by terminal restriction fragment length polymorphism with 4 primer-restriction enzyme systems, and the 120 obtained operational taxonomic units (OTUs) were analyzed by Data mining software focusing on the following 5 characteristics, namely, age, body mass index, present smoking habit, cessation period of previous smokers and drinking habit, according to the answers of the subjects. After performing Data mining analyses with each characteristic, the details of the constructed Decision trees precisely identified the subjects or discriminated them into various suitable groups. Through the pathways to reach the groups, practical roles of the related OTUs and their quantities were clearly recognized. Compared with the other identification methods for OTUs such as bicluster analyses, correlation coefficients and principal component analyses, the clear difference of this Data mining technique was that it set aside most OTUs and emphasized only some closely related ones. For example for a selected characteristic, such as smoking habit, only 7 OTUs out of 120 were able to identify all smokers, and the remaining 113 OTUs were thought of as data noise for smoking. Data mining analyses were affirmed as an effective method of subject discrimination for various physiological constitutions. The species of bacteria that were closely related to heavy smokers, i.e., HaeIII-291, were also discussed.

Hydrogenated resistant maltodextrin (H-RMD) is a dietary fiber whose energy value has not previously been reported. We evaluated the energy value of H-RMD. We conducted an in vitro digestion test, in vivo blood glucose measurement after ingestion, in vitro fermentability test, excretion test by rats and indirect calorimetry combined with breath hydrogen measurement for humans. H-RMD was hydrolyzed in vitro in a very small amount by human salivary amylase and by the rat small intestinal mucosal enzyme. Ingestion of H-RMD did not increase the blood glucose level of human subjects. An examination of in vitro fermentability suggested that H-RMD was fermented by several enterobacteria. Oral administration of H-RMD showed a saccharide excretion ratio of 42% by rats. A combination of indirect calorimetry and breath hydrogen measurement evaluated the metabolizable energy of H-RMD as 1.1 kcal/g in humans. We concluded from these results that H-RMD was not digested or absorbed in the upper gastrointestinal tract and was fermented in the colon to produce short-chain fatty acids which provided a lower amount of energy than that of resistant maltodextrin.

Resistant maltodextrin (RM) is a soluble dietary fiber that although resistant to digestion by human enzymes is a substrate for fermentation by the commensal microbiota of the large intestine. We d...

BACKGROUND The glycemic response to diet has been linked with noncommunicable diseases and is reduced by low-palatable, viscous, soluble fiber (1). Whether a palatable, low-viscous, soluble fiber such as resistant maltodextrin (RMD) has the same effect is unclear. OBJECTIVE The objective was to assess evidence on the attenuation of the blood glucose response to foods by < or = 10 g RMD in healthy adults. DESIGN We conducted a systematic review of randomized, placebo-controlled trials with the use of fixed- and random-effects meta-analyses and meta-regression models. RESULTS We found data from 37 relevant trials to April 2007. These trials investigated the attenuation of the glycemic response to rice, noodles, pastry, bread, and refined carbohydrates that included 30-173 g available carbohydrate. RMD was administered in drinks or liquid foods or solid foods. Placebo drinks and foods excluded RMD. Percentage attenuation was significant, dose-dependent, and independent of the amount of available carbohydrate coingested. Attenuation of the glycemic response to starchy foods by 6 g RMD in drinks approached approximately 20%, but when placed directly into foods was approximately 10% -- significant (P < 0.001) by both modes of administration. Study quality analyses, funnel plots, and trim-and-fill analyses uncovered no cause of significant systematic bias. Studies from authors affiliated with organizations for-profit were symmetrical without heterogeneity, whereas marginal asymmetry and significant heterogeneity arose among studies involving authors from nonprofit organizations because of some imprecise studies. CONCLUSIONS A nonviscous palatable soluble polysaccharide can attenuate the glycemic response to carbohydrate foods. Evidence of an effect was stronger for RMD in drinks than in foods.

As the physiological functions of soluble dietary fibre, the favourable efficacy, such as attenuating the absorption of saccharides or lipids, is expected. Resistant maltodextrin, a soluble dietary fibre, was investigated and found that it delays the glucose absorption and attenuates the postprandial rise in the blood glucose levels, however, the efficacy of resistant maltodextrin on lipid metabolism is not yet reported. We conducted an animal experiment and a human experiment to investigate the effect of resistant maltodextrin on postprandial blood triacylglycerol elevation. 1. Rats were fed corn oil with or without resistant maltodextrin and the postprandial changes in triacylglycerol were examined. 2. We then conducted a dietary loading experiment on 13 healthy adult male and female subjects using a meal containing approximately 50 g fat. A beverage not containing resistant maltodextrin was used as a placebo; subjects consumed the loading meal and a beverage containing either 5 g or 10 g resistant maltodextrin; blood was periodically collected to see the changes in serum constituents. 1. The corn oil administration experiment using rats showed that resistant maltodextrin dose-dependently suppressed elevation of blood triacylglycerol levels after corn oil administration. 2. The dietary loading experiment on 13 healthy subjects with 5 or 10 g of resistant maltodextrin showed that; in each administration group, resistant maltodextrin significantly suppressed postprandial elevation of blood triacylglycerol, RLP-cholesterol and insulin. These results indicate that resistant maltodextrin ingested with fatty meals suppresses the postprandial elevation of blood triacylglycerol levels.

Determination of the metabolizable (ME) and net metabolizable (NME) energy of total carbohydrate requires estimation of its available (AC) and fermentable (FC) carbohydrate content. Modeling of indirect calorimetric observations (respiratory gas exchange) and breath hydrogen would appear to make it possible to estimate noninvasively these nutritional quantities and the approximate time-course of availability.We assessed the time-course of metabolism and energy availability from resistant maltodextrin (RMD) by modeling of respiratory gases after a single oral dose.Seventeen healthy adults (13 M, 4 F; aged 25-46 y) were randomly assigned to treatments (water, maltodextrin, or RMD) in a multiple-crossover, single-blinded trial withor = 7 d washout. We monitored 8-h nitrogen-corrected oxygen and carbon dioxide exchanges and breath hydrogen. All treatment groups took low-carbohydrate meals at 3 and 6 h.Indirect calorimetry alone provided only qualitative information about the nutritional values of carbohydrate. In contrast, modeling of gaseous exchanges along with the use of central assumptions showed that 17 +/- 2% of RMD was AC and 40 +/- 4% was FC. As compared with 17 kJ gross energy/g RMD, mean (+/- SE) energy values were 7.3 +/- 0.6 kJ ME/g and 6.3 +/- 0.5 kJ NME/g. The fiber fraction of RMD provided 5.2 +/- 0.7 kJ ME/g and 4.1 +/- 0.6 kJ NME/g.Modeling with the use of this noninvasive and widely available respiratory gas-monitoring technique yields nutritional values for carbohydrate that are supported by enzymatic, microbial, and animal studies and human fecal collection studies. Improvement in this approach is likely and testable across laboratories.

We investigated the effects of selective beta 1 adrenoceptor stimulation on oxygen tension (pO2) in the myocardium of anesthetized dogs. A beta 1-selective full agonist, T-0509 (0.01-0.05 microgram/kg, i.v.), caused positive inotropic and chronotropic effects, and increased left circumflex blood flow, although it did not change arterial blood pressure. These effects were inhibited by bisoprolol (10 micrograms/kg), but not by ICI 118551 (30 micrograms/kg). Under control conditions, subepicardial pO2 (pO2 epi) and subendocardial pO2 (pO2endo) were approximately 33 and 27 mmHg, respectively. T-0509 (0.05 microgram/kg) decreased pO2epi in all cases, with a mean decrease of 2.6 +/- 0.5 mmHg, and this was significantly inhibited by bisoprolol. T-0509 caused an increase (7 out of 10 dogs) or a slight decrease (3 out of 10) in the pO2endo; the mean increment was 2.0 +/- 1.3 mmHg (n = 10). Isoproterenol (0.01-0.05 microgram/kg, i.v.) exerted positive inotropic and chronotropic effects that were sensitive to bisoprolol, and a hypotensive effect that was sensitive to ICI 118551. Isoproterenol caused an increase in blood flow that was sensitive to ICI 118551. Isoproterenol (0.05 microgram/kg) decreased pO2epi in all cases, with a mean decrease of 2.7 +/- 0.5 mmHg, which was significantly inhibited by bisoprolol. Isoproterenol caused an increase (5 out of 10) or a slight decrease (5 out of 10) in the pO2endo; the mean increment was 1.1 +/- 1.2 mmHg (n = 10).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of TKG01 on gastric ulcers and gastric secretion in rats were investigated in comparison with those of TA903, which is the equimolar clathrate compound of TKG01 anhydride with beta-cyclodextrin. The doses were adjusted on a molecular weight basis to include the same amount of TKG01 anhydride. Water-immersion stress ulcers were dose-dependently (100, 300 mg/kg) inhibited by TA903 given orally, but only significantly inhibited by TKG01 (300 mg/kg). TA903, given orally, even in low doses (30, 100 mg/kg) potently inhibited HCl-ethanol ulcers, whereas TKG01 did not inhibit these ulcers. Both TA903 and TKG01, given orally (100, 300 mg/kg), showed similar inhibition of indomethacin ulcers. TA903, given intraduodenally (100, 300 mg/kg), dose-dependently inhibited gastric secretion (volume, acid output and pepsin output) in pylorus-ligated rats, but TKG01 only inhibited pepsin output (100, 300 mg/kg). These results showed that TA903 had a broader spectrum of anti-ulcer effects than TKG01 and the mechanism of TA903 could involve both its cytoprotective activity and its anti-secretory effect.