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. 2023 Mar 20;8:132. doi: 10.1038/s41392-023-01399-3

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Schematic summary of interactions of bile acids and gut microbe participate in the host metabolism. Note: BAs, bile acids; BSEP, bile salt export protein; FGF, fibroblast growth factor; FGFR, FGF receptor; RXR, retinoid X receptor; NTCP, sodium taurocholate cotransporting polypeptide; OATP, organic anion-transporting polypeptide; SHP, small heterodimer partner; JNK, c-Jun N-terminal kinase; ERK, extracellular signal-regulated kinase; T3, thyroid hormone; T4, thyroxine; DIO2, type 2 iodothyronine deiodinase; ASBT, apical sodium-dependent bile acid transporter; OST, organic solute transporter. Primary bile acids are synthesized and then conjugated with taurine or glycine in hepatocytes. Conjugated bile acids are transported into the bile duct by BSEP. Most conjugated bile acids are reabsorbed via ASBT and circulate to the liver by OATP, OSTa/b, and NTCP. Bile acids acts as the endogenous ligands for FXR and TGR5 to generate distinct effects on metabolism regulation. The figures created by BioRender