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The bile acid metabolic pathway is a complex network of biochemical reactions and signaling events governing the synthesis, conjugation, transport, enterohepatic circulation, and regulation of bile acids—detergent-like molecules essential for digestion and absorption of dietary fats and fat-soluble vitamins. Beyond their classic role in lipid metabolism, bile acids act as ligands for a range of cell-surface and nuclear receptors, including FXR (Farnesoid X receptor), TGR5 (G protein–coupled bile acid receptor), and others, thereby linking metabolism to immune modulation, inflammation, and disease. Disruption or abnormal regulation of this pathway is implicated in a spectrum of diseases ranging from liver and metabolic syndromes to inflammatory bowel disease and cancer. Therapeutic strategies do not target the “pathway” per se but rather enzymes, transporters (e.g., ASBT, NTCP), or receptors (e.g., FXR, TGR5) that mediate crucial steps within this pathway. Modulation of bile acid pools via drugs or dietary interventions is under intense research as a means to manage liver disorders, metabolic disease, and systemic inflammation. Note: This entry refers to a biological pathway, not a single molecular target. For drug targeting or biochemical studies, refer to specific molecules such as "Farnesoid X receptor (FXR)", "ASBT", "TGR5", etc. The information above facilitates mapping to more granular, actionable targets as needed for therapeutic development.
FXR agonism (activated by OCA and some bile acids). TGR5 agonism (targeting metabolic and inflammatory pathways). Inhibition of bile acid transporters (ASBT, NTCP). Modulation of gut microbiota influencing bile acid pool composition. Bile acid sequestration (resins e.g., cholestyramine).
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