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Microbial modulation of energy availability in the colon regulates intestinal transit.

Journal article
Authors Anita Wichmann
Ava Allahyar
Thomas U. Greiner
Hubert Plovier
Gunnel Östergren Lundén
Thomas Larsson
Daniel J Drucker
Nathalie M Delzenne
Patrice D Cani
Fredrik Bäckhed
Published in Cell host & microbe
Volume 14
Issue 5
Pages 582-90
ISSN 1934-6069
Publication year 2013
Published at Wallenberg Laboratory
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 582-90
Language en
Subject categories Basic Medicine


Gut microbiota contribute to host metabolic efficiency by increasing energy availability through the fermentation of dietary fiber and production of short-chain fatty acids (SCFAs) in the colon. SCFAs are proposed to stimulate secretion of the proglucagon (Gcg)-derived incretin hormone GLP-1, which stimulates insulin secretion (incretin response) and inhibits gastric emptying. We find that germ-free (GF) and antibiotic-treated mice, which have severely reduced SCFA levels, have increased basal GLP-1 levels in the plasma and increased Gcg expression in the colon. Increasing energy supply, either through colonization with polysaccharide-fermenting bacteria or through diet, suppressed colonic Gcg expression in GF mice. Increased GLP-1 levels in GF mice did not improve the incretin response but instead slowed intestinal transit. Thus, microbiota regulate the basal levels of GLP-1, and increasing these levels may be an adaptive response to insufficient energy availability in the colon that slows intestinal transit and allows for greater nutrient absorption.

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