Changes of fermentation pathways of fecal microbial communities associatedwith a drug treatment that increases dietary starch in the human colon

Acarbose inhibits starch digestion in the human small intestine. This incre ases the amount of starch available for microbial fermentation to acetate, propionate, and butyrate in the colon. Relatively large amounts of butyrate are produced from starch by colonic microbes. Colonic epithelial cells use butyrate as an energy source, and butyrate causes the differentiation of c olon cancer cells, In this study we investigated whether colonic fermentati on pathways changed during treatment with acarbose, We examined fermentatio ns by fecal suspensions obtained from subjects who participated in an acarb ose-placebo crossover trial. After incubation with [1-C-13] glucose and (CO 2)-C-12 or with unlabeled glucose and (CO2)-C-13, the distribution of C-13 in product C atoms was determined by nuclear magnetic resonance spectrometr y and gas chromatography-mass spectrometry. Regardless of the treatment, ac etate, propionate, and butyrate were produced from pyruvate formed by the E mbden-Meyerhof-Parnas pathway. Considerable amounts of acetate were also fo rmed by the reduction of CO2. Butyrate formation from glucose increased and propionate formation decreased with acarbose treatment, Concomitantly, the amounts of CO2 reduced to acetate were 30% of the total acetate in untreat ed subjects and 17% of the total acetate in the treated subjects. The aceta te, propionate, and butyrate concentrations were 57, 20, and 23% of the tot al final concentrations, respectively, for the untreated subjects and 57, 1 3, and 30% of the total final concentrations, respectively, for the treated subjects.