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. 2021 Sep 23;11:729346. doi: 10.3389/fcimb.2021.729346

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Copyright © 2021 Xiao, Liu, Luo and Xiong

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Host-microbiota interactions during bile-acid metabolism. In homeostasis, primary bile acids are converted into secondary bile acids with the assistance of intestinal flora and Takeda-G-protein-receptor-5 (TGR5) (see the figure, part A). Gut microbiota alterations induce an impairment in the ileal absorption of BAs, which occurs normally via the apical-sodium BA transporter (ASBT). This induces a decrease in the expression of nuclear Farnesoid-X receptor (FXR) and fibroblast growth factor 19 (FGF19) in intestinal epithelial cells and the abundance of colonic primary conjugated BAs. Gut microbiota dysfunction leads to a decreased transformation of primary conjugated BAs to secondary BAs in the colon, leading to defective activation of (TGR5). TGR5 of glucagon-like peptide 1 (GLP-1) activation effect was thus inhibited (see the figure, part B).