Bile acid pool and biliary cholesterol (BA pool)

The bile acid pool and biliary cholesterol represent a critical physiological compartment involved in lipid digestion and systemic cholesterol homeostasis [1.2.1, 1.2.3]. Bile acids, synthesized from cholesterol in the liver, are secreted into the bile and cycle through the enterohepatic circulation, where they facilitate the emulsification and absorption of dietary fats and fat-soluble vitamins [1.2.2, 1.7.3]. Biliary cholesterol is the primary route for the body to eliminate excess cholesterol, and its solubility is maintained by the presence of bile acids and phospholipids [1.1.3, 1.2.3]. Dysregulation of this pool, such as an overabundance of hydrophobic bile acids or supersaturation of cholesterol, leads to pathologies including cholestasis, gallstones, and hyperlipidemia [1.7.1, 1.7.4]. Therapeutic strategies targeting this system include bile acid sequestrants and IBAT inhibitors that interrupt recycling to lower systemic cholesterol or reduce cholestatic symptoms, as well as agents like ezetimibe that specifically inhibit the reabsorption of biliary cholesterol [1.1.2, 1.6.1, 1.6.2]. Additionally, bile acids act as signaling molecules through receptors like FXR and TGR5, making the pool a central hub for metabolic regulation [1.4.3, 1.7.2].

Other names

Enterohepatic bile acid poolBiliary lipid poolBile salt poolBiliary cholesterol poolEnterohepatic circulation

Drugs modulate the bile acid pool and biliary cholesterol through several mechanisms: bile acid sequestrants bind bile acids in the intestinal lumen to prevent reabsorption [1.6.3]; IBAT inhibitors block the apical sodium-dependent bile acid transporter (ASBT) to interrupt enterohepatic circulation [1.6.2]; cholesterol absorption inhibitors like ezetimibe target NPC1L1 to reduce the uptake of biliary and dietary cholesterol [1.1.2]; and bile acid derivatives like UDCA modify the pool's composition to reduce toxicity or activate regulatory receptors like FXR [1.4.2, 1.6.1].