Bile acid is a host factor that regulates the composition of the cecal microbiota in rats.

Abstract:

BACKGROUND & AIMS:Alterations in the gastrointestinal microbiota have been associated with metabolic diseases. However, little is known about host factors that induce changes in gastrointestinal bacterial populations. We investigated the role of bile acids in this process because of their strong antimicrobial activities, specifically the effects of cholic acid administration on the composition of the gut microbiota in a rat model. METHODS:Rats were fed diets supplemented with different concentrations of cholic acid for 10 days. We used 16S ribosomal RNA gene clone library sequencing and fluorescence in situ hybridization to characterize the composition of the cecal microbiota of the different diet groups. Bile acids in feces, organic acids in cecal contents, and some blood parameters were also analyzed. RESULTS:Administration of cholic acid induced phylum-level alterations in the composition of the gut microbiota; Firmicutes predominated at the expense of Bacteroidetes. Cholic acid feeding simplified the composition of the microbiota, with outgrowth of several bacteria in the classes Clostridia and Erysipelotrichi. Externally administered cholic acid was efficiently transformed into deoxycholic acid by a bacterial 7α-dehydroxylation reaction. Serum levels of adiponectin decreased significantly in rats given the cholic acid diet. CONCLUSIONS:Cholic acid regulates the composition of gut microbiota in rats, inducing similar changes to those induced by high-fat diets. These findings improve our understanding of the relationship between metabolic diseases and the composition of the gastrointestinal microbiota.

journal_name

Gastroenterology

journal_title

Gastroenterology

authors

Islam KB,Fukiya S,Hagio M,Fujii N,Ishizuka S,Ooka T,Ogura Y,Hayashi T,Yokota A

doi

10.1053/j.gastro.2011.07.046

subject

Has Abstract

pub_date

2011-11-01 00:00:00

pages

1773-81

issue

5

eissn

0016-5085

issn

1528-0012

pii

S0016-5085(11)01081-X

journal_volume

141

pub_type

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