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The metabolic activity of fecal microbiota from healthy individuals and patients with inflammatory bowel disease

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Author: Nuenen, M.H.M.C. van · Venema, K. · Woude, J.C.J. van der · Kuipers, E.J.
Institution: TNO Voeding
Source:Digestive Diseases and Sciences, 3, 49, 485-491
Identifier: 237660
doi: doi:10.1023/B:DDAS.0000020508.64440.73
Keywords: Nutrition · Physiological Sciences · Fermentation · In vitro model · Inflammatory bowel disease · Metabolites · Microbial activity · ammonia · branched chain fatty acid · fatty acid · lactic acid · phenol derivative · short chain fatty acid · unclassified drug · adult · article · carbohydrate metabolism · chronicity · clinical article · controlled study · enteritis · fatty acid synthesis · feces microflora · fermentation · human · in vitro study · metabolite · microbial metabolism · model · nonhuman · normal human · priority journal · protein degradation · Adult · Ammonia · Bacteria · Colitis, Ulcerative · Colon · Crohn Disease · Fatty Acids · Fatty Acids, Volatile · Feces · Fermentation · Humans · Lactic Acid · Middle Aged


The hypothesis was studied that intestinal microbial metabolites play a role in the pathogenesis of inflammatory bowel disease. For that purpose, an in vitro model of the colon was inoculated with fresh feces of six healthy individuals and eight inflammatory bowel disease patients. Samples were taken from the model over time to analyze metabolites from both saccharolytic and proteolytic fermentation. Microbiotas from inflammatory bowel disease patients produced significantly more short-chain fatty acids and ammonia than microbiotas from healthy individuals. Furthermore, the branched-chain fatty acid production was 25% higher after inoculation with microbiotas from patients than after inoculation with microbiotas from healthy individuals. Phenolic compounds were produced by all microbiotas, with large interindividual variation. The production of (potentially toxic) metabolites may play a role in the onset or chronicity of inflammatory bowel disease, because they were produced in higher amounts by microbiotas from these patients than by microbiotas from healthy individuals.