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In recent years, there have been many reports on the effects of prebiotics on intestinal health. In particular, the consumption of resistant maltodextrin (RMD) has been reported to be beneficial. However, there has been no comprehensive quantification of the effect of RMD on the intestinal environment. Therefore, this study aimed to quantify the effects of RMD on the intestine, especially the intestinal microbiome and metabolome profiles. A randomized, double-blind, and controlled trial was conducted in 29 Japanese subjects, whose hemoglobin A1c (HbA1c) levels are larger than 6% (Clinical trial no. UMIN000023970, https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000027589). The subjects consumed RMD or placebo twice per day for 24 weeks. Blood and fecal samples were collected before and after the intake. The intestinal environment was assessed by a metabologenomics approach, involving 16S rRNA gene-based microbiome analysis and mass spectrometry-based metabolome analysis. The intake of RMD increased the levels of Bifidobacterium and Fusicatenibacter and decreased deoxycholate levels. Additionally, intake of RMD lowered the levels of some opportunistic virulent metabolites, such as imidazole propionate and trimethylamine, in subjects with an initially high amount of those metabolites. RMD may have beneficial effects on the gut environment, such as commensal microbiota modulation and reduction of virulence metabolites, which is known as a causative factor in metabolic disorders. However, the effects of RMD partially depend on the gut environmental baseline.

ObjectiveIn recent years, there have been many reports on the effects of prebiotics on intestinal health. In particular, consuming resistant maltodextrin (RMD) has been reported to be beneficial. However, there has been no comprehensive quantification of the effect of RMD on the intestinal environment. Therefore, this study aimed to quantify the effects of RMD on the intestine, especially the intestinal microbiome and metabolome profiles.DesignA randomized, double-blind controlled trial was conducted in 29 Japanese subjects with relatively high hemoglobin A1c (HbA1c). Subjects consumed RMD or placebo twice per day for 24 weeks. Blood and fecal samples were collected before and after intake. The intestinal environment was assessed by a metabologenomics approach combined with 16S rRNA gene-based microbiome and mass spectrometry-based metabologenomics analyses.ResultsThe intake of RMD increased the levels of Bifidobacterium and Fusicatenibacter, and decreased deoxycholate. In addition, intake of the RMD lowered the levels of some virulent metabolites, such as imidazole propionate and trimethylamine, in subjects with an initially high amount of those metabolites.ConclusionRMD may have beneficial effects on the gut environment such as commensal microbiota modulation and reduction of virulence metabolites, known as a causative factor in metabolic disorders. However, its effect partially depends on the gut environmental baseline.

Resistant maltodextrin (RMD) is a soluble dietary fibre that exerts several physiological functions as a result of its microbial degradation and changes in the intestinal environment. It has been reported that RMD enhanced immunoglobulin A (IgA) secretion, which protects the mucosa from foreign substances. However, the effect of RMD on excessive immunity has yet to be investigated. In this study, we aimed to investigate the effect of RMD on excessive immune responses such as food allergy. OVA23-3 mice were fed an AIN-76-based diet containing 20% egg-white protein with or without RMD. While RMD was shown to contribute to an increase in goblet cells, RMD did not change the overall inflammatory status when ingested with the egg-white diet. RMD suppressed IL-4 and IL-10 production from splenocytes but not cells from mesenteric lymph nodes. RMD also downregulated the serum levels of OVA-specific Th1- and Th2-related antibodies, which were elevated in the food-allergic condition. RMD significantly increased the total amount of short-chain fatty acids, especially acetate and propionate, in the caecum of OVA23-3 mice fed the egg-white diet. Our study demonstrated that dietary RMD modulates systemic rather than intestinal antigen-specific immune responses in the food-allergic condition of OVA23-3 mice. Although the relevant mechanism has yet to be investigated, RMD shows potential for alleviating food allergy through adjustment of systemic immunity.

Experiments with rats have produced data on the metabolism and energy value of d-psicose; however, no such data have been obtained in humans. The authors assessed the availability of d-psicose absorbed in the small intestine by measuring carbohydrate energy expenditure (CEE) by indirect calorimetry. They measured the urinary excretion rate by quantifying d-psicose in urine for 48 hours. To examine d-psicose fermentation in the large intestine, the authors measured breath hydrogen gas and fermentability using 35 strains of intestinal bacteria. Six healthy subjects participated in the CEE test, and 14 participated in breath hydrogen gas and urine tests. d-Psicose fermentation subsequent to an 8-week adaptation period was also assessed by measuring hydrogen gas in 8 subjects. d-Psicose absorbed in the small intestine was not metabolized into energy, unlike glucose, because CEE did not increase within 3 hours of d-psicose ingestion (0.35 g/kg body weight [BW]). The accumulated d-psicose urinary excretion rates were around 70% for 0.34, 0.17, and 0.08 g/kg BW of ingested d-psicose. Low d-psicose fermentability was observed in intestinal bacteria and breath hydrogen gas tests, in which fructooligosaccharide (0.34, 0.17, and 0.08 g/kg BW) was used as a positive control because its available energy is known to be 8.4 kJ/g. Based on the results of the plot of breath hydrogen concentration vs calories ingested, the energy value of d-psicose was expected to be less than 1.6 kJ/g. Incremental d-psicose fermentability subsequent to an adaptation period was not observed.

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.

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.