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Bile acid binding/sequestration refers to the process by which proteins or synthetic agents interact with bile acids, either to regulate their intracellular trafficking and detoxification (by intracellular lipid binding proteins, such as bile acid binding proteins or BABPs) or to reduce their intestinal reabsorption (by oral bile acid sequestrant drugs). BABPs are a family of cytosolic proteins critical for buffering and trafficking bile acids within hepatocytes and enterocytes, thereby protecting cells from bile acid toxicity and maintaining homeostasis. In clinical therapy, synthetic bile acid sequestrants such as cholestyramine act by binding bile acids in the gut, preventing their enterohepatic recirculation and lowering cholesterol levels as a result.
Endogenous BABPs bind and shield bile acids intracellularly, modulating trafficking and buffering, and preventing cytotoxicity. Sequestrants bind bile acids in the intestine, preventing reabsorption, promoting fecal excretion, and lowering cholesterol.
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