Document Detail


Enterobacteria modulate intestinal bile acid transport and homeostasis through apical sodium-dependent bile acid transporter (SLC10A2) expression.
MedLine Citation:
PMID:  20884752     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In our study, ampicillin (AMP)-mediated decrease of enterobacteria caused increases in hepatic bile acid concentration through (at least in part) elevation of bile acid synthesis in C57BL/6N mice. We investigated the involvement of enterobacteria on intestinal bile acid absorption in AMP-treated mice in the present study. Fecal enterobacterial levels and fecal bile acid excretion rates were markedly decreased in mice treated with AMP (100 mg/kg) for 3 days, whereas bile acid concentrations in portal blood were significantly increased compared with those in mice treated with a vehicle. Ileal apical sodium-dependent bile acid transporter (SLC10A2) mRNA levels and ileal SLC10A2 protein levels in brush-border membranes were significantly increased compared with those in mice treated with the vehicle. In AMP-treated mice, total bile acid levels were increased, whereas levels of enterobacteria-biotransformed bile acid, taurodeoxycholic acid, and cholic acid were decreased in intestinal lumen. These phenomena were also observed in farnesoid X receptor-null mice treated with AMP for 3 days. Discontinuation of AMP administration after 3 days (vehicle administration for 4 days) increased levels of fecal enterobacteria, fecal bile acid excretion, and taurodeoxycholic acid and cholic acid in the intestinal lumen, whereas the discontinuation decreased ileal SLC10A2 expression and bile acid concentrations in the portal blood. Coadministration of taurodeoxycholic acid or cholic acid decreased ileal SLC10A2 expression in mice treated with AMP. These results suggest that enterobacteria-mediated bile acid biotransformation modulates intestinal bile acid transport and homeostasis through down-regulation of ileal SLC10A2 expression.
Authors:
Masaaki Miyata; Hiroki Yamakawa; Mayumi Hamatsu; Hideaki Kuribayashi; Yuki Takamatsu; Yasushi Yamazoe
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-09-30
Journal Detail:
Title:  The Journal of pharmacology and experimental therapeutics     Volume:  336     ISSN:  1521-0103     ISO Abbreviation:  J. Pharmacol. Exp. Ther.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-16     Completed Date:  2011-01-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376362     Medline TA:  J Pharmacol Exp Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  188-96     Citation Subset:  IM    
Affiliation:
Division of Drug Metabolism and Molecular Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3, Aoba, Aramaki, Aoba-ku, Sendai, 980-8578, Japan. miyata@mail.pharm.tohoku.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Ampicillin / pharmacology
Animals
Bile Acids and Salts / metabolism*
Biological Transport / drug effects,  physiology
Down-Regulation / drug effects,  physiology*
Enterobacteriaceae / drug effects,  physiology*
Homeostasis / drug effects,  physiology*
Ileum / metabolism*
Intestines / metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Organic Anion Transporters, Sodium-Dependent / biosynthesis*
Sodium / metabolism*
Symporters / biosynthesis*
Chemical
Reg. No./Substance:
0/Bile Acids and Salts; 0/Organic Anion Transporters, Sodium-Dependent; 0/Symporters; 145420-23-1/sodium-bile acid cotransporter; 69-53-4/Ampicillin; 7440-23-5/Sodium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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