Yuka Kishimoto

Failure of d-psicose absorbed in the small intestine to metabolize into energy and its low large intestinal fermentability in humans

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.

Continuous intake of resistant maltodextrin enhanced intestinal immune response through changes in the intestinal environment in mice

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.

Energy Value Evaluation of Hydrogenated 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.

Secretion of GLP-1 but not GIP is potently stimulated by luminal d -Allulose ( d -Psicose) in rats

Glucagon-like peptide 1 (GLP-1), an incretin gastrointestinal hormone, is secreted when stimulated by nutrients including metabolizable sugars such as glucose and fructose. d-Allulose (allulose), also known as d-psicose, is a C-3 isomer of d-fructose and a rare sugar with anti-diabetic or anti-obese effects in animal models. In the present study, we examined whether an oral administration of allulose could stimulate GLP-1 secretion in rats, and investigated the underlying mechanisms. Oral, but not intraperitoneal, administration of allulose (0.5-2.0 g/kg body weight) elevated plasma GLP-1 levels for more than 2 h in a dose-dependent manner. The effects of allulose on GLP-1 secretion were higher than that of dextrin, fructose, or glucose. In addition, oral allulose increased total and active GLP-1, but not glucose-dependent insulinotropic polypeptide (GIP), levels in the portal vein. In anesthetized rats equipped with a portal catheter, luminal (duodenum and ileum) administration of allulose increased portal GLP-1 levels, indicating the luminal effect of allulose. Allulose-induced GLP-1 secretion was abolished in the presence of xanthohumol (a glucose/fructose transport inhibitor), but not in the presence of inhibitors of the sodium-dependent glucose cotransporter 1 or the sweet taste receptor. These results demonstrate a potent and lasting effect of orally administered allulose on GLP-1 secretion in rats, without affecting GIP secretion. The potent and selective GLP-1-releasing effect of allulose holds promise for the prevention and treatment of glucose intolerance through promoting endogenous GLP-1 secretion.