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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.

BackgroundIt 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 studyWe conducted balance studies in rats to investigate effects of resistant maltodextrin and hydrogenated resistant maltodextrin on apparent mineral absorption.MethodsIn 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.ResultsIn 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.ConclusionIngestion 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.

We investigated the effect of resistant maltodextrin (RMD), a non-viscous soluble dietary fiber, on intestinal immune response and its mechanism in mice. Intestinal and fecal immunoglobulin A (IgA) were determined as indicators of intestinal immune response, and changes in the intestinal environment were focused to study the mechanism. BALB/c mice were fed one of three experimental diets, a control diet or a diet containing either 5% or 7.5% RMD, for two weeks. Continuous intake of RMD dose-dependently increased total IgA levels in the intestinal tract. Total IgA production from the cecal mucosa was significantly increased by RMD intake, while there were no significant differences in mucosal IgA production between the control group and experimental groups in the small intestine and colon. Continuous intake of RMD changed the composition of the cecal contents; that is, the composition of the cecal microbiota was changed, and short-chain fatty acids (SCFAs) were increased. There was an increased trend in Bacteroidales in the cecal microbiota, and butyrate, an SCFA, was significantly increased. Our study demonstrated that continuous intake of RMD enhanced the intestinal immune response by increasing the production of IgA in the intestinal tract. It suggested that the increase in total SCFAs and changes in the intestinal microbiota resulting from the fermentation of RMD orally ingested were associated with the induction of IgA production in intestinal immune cells, with the IgA production of the cecal mucosa in particular being significantly increased.

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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.

Objective: In 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. Design: A 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. Results: The 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. Conclusion: RMD 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.

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.