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

Acarbose inhibits starch digestion in the human small intestine. This increases 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...

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Published inApplied and Environmental Microbiology Vol. 65; no. 7; pp. 2807 - 2812
Main Authors Wolin, M.J, Miller, T.L, Yerry, S, Zhang, Y, Bank, S, Weaver, G.A
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.07.1999
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Summary:Acarbose inhibits starch digestion in the human small intestine. This increases 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 colon cancer cells. In this study we investigated whether colonic fermentation pathways changed during treatment with acarbose. We examined fermentations by fecal suspensions obtained from subjects who participated in an acarbose-placebo crossover trial. After incubation with [1-(13)C]glucose and (12)CO(2) or with unlabeled glucose and 13CO(2), the distribution of (13)C in product C atoms was determined by nuclear magnetic resonance spectrometry and gas chromatography-mass spectrometry. Regardless of the treatment, acetate, propionate, and butyrate were produced from pyruvate formed by the Embden-Meyerhof-Parnas pathway. Considerable amounts of acetate were also formed by the reduction of CO(2). Butyrate formation from glucose increased and propionate formation decreased with acarbose treatment. Concomitantly, the amounts of CO(2) reduced to acetate were 30% of the total acetate in untreated subjects and 17% of the total acetate in the treated subjects. The acetate, propionate, and butyrate concentrations were 57, 20, and 23% of the total final concentrations, respectively, for the untreated subjects and 57, 13, and 30% of the total final concentrations, respectively, for the treated subjects.
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Corresponding author. Mailing address: Wadsworth Center for Laboratories and Research, New York State Department of Health, Empire State Plaza Box 509, Albany, NY 12201-0509. Phone: (518) 474-1909. Fax: (518) 474-8590. E-mail: meyer.wolin@wadsworth.org.
ISSN:0099-2240
1098-5336
DOI:10.1128/aem.65.7.2807-2812.1999