Bile acid metabolic disorders and their role in hepatic encephalopathy of cirrhosis

Figure 2 Bile acid synthesis, transformation, reabsorption, and negative feedback regulation. In the liver, cholesterol undergoes a series of enzymatic reactions to produce primary bile acids (BAs), which then enter the intestine and are converted into secondary BAs. Both primary and secondary BAs can conjugate with glycine or taurine. Most BAs are eventually reabsorbed into the bloodstream, with only a small portion excreted in feces. This process is negatively regulated by small heterodimer partner and intestine-derived fibroblast growth factor 15/19. FGFR4: Fibroblast growth factor receptor 4; GCA: Glycocholic acid; GCDCA: Glycochenodeoxycholic acid; BAs: Bile acids; CYP7A1: Cholesterol 7α-hydroxylase; CYP8B1: Sterol 12α-hydroxylase; CYP27A1: Sterol 27-hydroxylase; CYP7B1: Oxysterol 7α-hydroxylase; CA: Cholic acid; CDCA: Chenodeoxycholic acid; BACS: Bile acid-CoA synthetase; BAAT: Bile acid-CoA: Amino acid N-acyltransferase; BSEP: Bile salt export pump; T: Taurine; G: Glycine; BSH: Bile salt hydrolase; HSD: Hydroxysteroid dehydrogenase; DCA: Deoxycholic acid; LCA: Lithocholic acid; ASBT: Apical sodium-dependent bile acid transporter; IBABP: Ileal bile acid-binding protein; OSTα/β: Organic solute transporter α/β; NTCP: Sodium taurocholate cotransporting polypeptide; FXR: Farnesoid X receptor; SHP: Small heterodimer partner; LRH-1: Liver receptor homolog-1; HNF-4α: Hepatocyte nuclear factor 4 α; FGF15/19: Fibroblast growth factor 15/19. The double upward arrows (↑↑) indicate elevated levels or increased expression. Created in BioRender.