Fructo-oligosaccharides (FOS) are a mixture of oligosaccharides consisting of glucose linked to fructose units. They are not digested in the human small intestine but fermented in the colon, where they could specifically promote the growth of some species of the indigenous microflora, especially bifidobacteria. We assessed in healthy humans the effects of FOS ingestion in fecal bifidobacteria and selected metabolic indexes potentially involved in colonic carcinogenesis. Twenty volunteers randomly divided into two groups were studied for three consecutive 12-day periods. During the ingestion period, they received 12.5 g/day FOS or placebo (saccharose) in three oral doses. Stools were regularly collected and analyzed. FOS ingestion led to an increase in fecal bifidobacterial counts [7.9 +/- 0.5 to 9.1 +/- 0.3 (SE) log colony-forming units/g wet wt, p < 0.01] and beta-fructosidase activity (9.6 +/- 1.9 to 13.8 +/- 1.9 IU/g dry wt, p < 0.01). In contrast, FOS ingestion had no significant effect on fecal total anaerobes, pH, the activities of nitroreductase, azoreductase, and beta-glucuronidase, and the concentrations of bile acids and neutral sterols. We conclude that ingestion of FOS, at a clinically tolerated dose of 12.5 g/day, led to an increase in colonic bifidobacteria. This effect was not associated in healthy humans with beneficial changes in various factors potentially involved in the pathogenesis of colonic cancer.
The fate of fructooligosaccharides (FOS) in the human gastrointestinal tract was evaluated in six healthy volunteers over an 11-d period. After an equilibration phase, 20.1 g FOS/d was given in three identical postprandial doses. Distal ileal output of FOS and their constituent components were determined by intestinal aspiration after a single meal, and the amounts of FOS excreted in stools and urine were also measured. Most of ingested FOS, 89 +/- 8.3% (mean +/- SEM), was not absorbed in the small intestine, and none was excreted in stools, indicating that the portion reaching the colon was completely fermented by colonic flora. A small fraction of ingested FOS was recovered in urine. The mean estimated energy value of FOS was 9.5 kJ/g. We conclude that in healthy humans, FOS are only slightly digested in the small intestine and then fermented in the colon, resulting in reduced energy production.
The capacity of CGTase for using bCD (beta cyclodextrin) as glucosyl donor and transferring it to sucrose molecules was investigated. We showed that this enzyme was able to produce polyglucosyl-fructosides (G n F) by a coupling reaction between bCD and sucrose. Maltooligosaccharides were also synthesised but in lesser amounts. The degree of polymerisation (DP) of the different products was limited to a value of 8 and this allowed us to purify all of them by size exclusion chromatography. Mass spectrometry and NMR analysis of the unknown products revealed that they consisted of linear maltooligosaccharides of various DP bound to the glucose moiety of a sucrose molecule by a a(10/4) linkage.
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