bile salts

Bile salts are formed in hepatocytes by conjugation of primary bile acids (cholic acid and chenodeoxycholic acid, synthesized from cholesterol via the rate-limiting enzyme cholesterol 7α-hydroxylase/CYP7A1) with glycine or taurine, making them more water-soluble and effective emulsifiers. Gut bacteria further convert primary bile acids into secondary bile acids (deoxycholic acid, lithocholic acid) via dehydroxylation. Bile salts are secreted into bile, stored and concentrated in the gallbladder, and released into the duodenum in response to CCK (triggered by fat and protein in the duodenum) to emulsify lipids, increasing surface area for pancreatic lipase action and forming micelles that facilitate absorption of fatty acids, monoglycerides, and fat-soluble vitamins (A, D, E, K) in the small intestine. About 95% of bile salts are reabsorbed in the terminal ileum via active transport (apical sodium-dependent bile acid transporter, ASBT) and recycled through enterohepatic circulation back to the liver; the remainder is excreted in feces. Clinical relevance: Bile salt deficiency (e.g., from cholestasis, ileal resection/disease like Crohn's, cirrhosis, or biliary obstruction) leads to fat malabsorption and steatorrhea, along with deficiencies in fat-soluble vitamins. Bile acid sequestrants (cholestyramine, colestipol) bind bile acids in the gut, interrupting enterohepatic circulation, promoting increased hepatic conversion of cholesterol to bile acids, and thereby lowering LDL cholesterol. Excess cholesterol relative to bile salts and phospholipids can lead to cholesterol gallstones. Bile salts are also important in preventing bacterial overgrowth in the small intestine.