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The taurine-conjugated bile acid metabolic pathway is a critical biochemical network in the liver and intestine responsible for the amidation of primary bile acids with the amino acid taurine. This process is primarily catalyzed by the enzymes bile acid-CoA ligase (BACS/SLC27A5) and bile acid-CoA:amino acid N-acyltransferase (BAAT), which convert cholic acid and chenodeoxycholic acid into their taurine-conjugated forms, such as taurocholic acid and taurochenodeoxycholic acid (1, 7, 13). These conjugates are essential for the emulsification and absorption of dietary lipids and fat-soluble vitamins due to their high solubility and detergent properties at physiological pH (3, 14). Beyond their role in digestion, taurine-conjugated bile acids serve as potent signaling molecules that activate nuclear receptors like the farnesoid X receptor (FXR) and membrane receptors such as G protein-coupled bile acid receptor 1 (TGR5) and sphingosine-1-phosphate receptor 2 (S1PR2), thereby regulating glucose, lipid, and energy homeostasis (2, 6, 11). Dysregulation of this pathway is implicated in various pathologies, including hepatocellular carcinoma, where elevated taurine-conjugated bile acids can promote tumor growth, and familial hypercholanemia, which results from genetic defects in BAAT (1, 10). Therapeutic strategies targeting this pathway include FXR agonists to restore bile acid homeostasis, IBAT inhibitors to reduce bile acid reabsorption, and bile acid sequestrants to lower cholesterol and manage cholestatic symptoms (6, 11, 13).
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