Table 2.

Potential mechanisms linking G protein-coupled bile acid receptor 1 (GPBAR-1) to bile acid (BA) pool composition [3,46].

Site/Pathway	Mechanism(s)
Liver (BA synthesis)	-Control of synthetic pathway [102] -GPBAR-1 KO (knockout) mice → decreased expression of Cyp7b1 gene (reduction of the alternative BA synthesis) → BA metabolism shifts towards the classic pathway→ assembly of more hydrophobic pool (also hepatic growth hormone-signal transducer and activator of transcription 5, Growth hormone (GH)/STAT5 signalling) [102]
Intestine (BA biotransformation)	-Activation of intestinal farnesoid X receptor (FXR) (e.g., FXR agonist fexaramine) might shape gut microbiota → increase of taurolitocholic acid (TLCA) → activation of intestinal GPBAR-1→ release of Glucagon-like peptide 1 (GLP-1) → improved hepatic glucose and insulin sensitivity and increased adipose tissue browning [91,92,103]
Enterohepatic cycle, ileum, biliary tract, kidney/transepithelial flux of BA	-Largely unknown -Regulation of BA transport in the gallbladder epithelial cells (namely, cholecysto-hepatic shunt) → decreased intestinal circulation of BA→ decreased biotransformation of primary to secondary BA → decreased hydrophobicity of the BA pool [104,105]