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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.

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.