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The taurine-conjugated bile acid metabolic pathway is a critical biochemical process in the liver and intestine that regulates the solubility, transport, and signaling properties of bile acids. In this pathway, primary bile acids synthesized from cholesterol are activated by bile acid-CoA ligase (BACS) and subsequently conjugated with the amino acid taurine by bile acid-CoA:amino acid N-acyltransferase (BAAT) [UniProt, NIH]. This amidation increases the hydrophilicity and acidity of bile acids, facilitating their secretion into bile and their role as detergents for dietary lipid absorption in the small intestine [NIH]. Beyond 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 TGR5 and S1PR2, thereby regulating glucose, lipid, and energy metabolism [NIH]. Dysregulation of this pathway is implicated in various pathologies, including cholestatic liver diseases, non-alcoholic steatohepatitis (NASH), and certain cancers, where altered bile acid profiles can promote inflammation or tumorigenesis [MDPI, NIH]. Therapeutic strategies targeting this pathway include FXR agonists, which suppress bile acid synthesis and promote transport, and IBAT inhibitors, which prevent the reabsorption of conjugated bile acids in the ileum [NIH].
Modulation of bile acid synthesis, transport, and signaling through FXR agonism, TGR5 activation, or IBAT inhibition.
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