Abstract
Biliary secretion is reviewed. Bile acids pass along the biliary tract and small intestine without undergoing passive absorption because of their hydrophilicity and size. Active ileal absorption leads to the development of a large circulating pool of molecules and thus dissociates biliary secretion from bile acid biosynthesis (which is synonymous with cholesterol degradation). Man differs from most vertebrates in having little bile acid-independent flow; bile acid-dependent flow is also less in man than many other vertebrates. The hypercholeretic effects of certain bile acids are reviewed; the most likely explanation is cholehepatic shunting of the unconjugated, lipophilic species. Biliary lipid secretion involves bile acid-stimulated microtubule-dependent movement of phospholipid-cholesterol-rich vesicles from the Golgi to the canaliculus. Bile acid biotransformation during hepatic transport involves reconjugation (with glycine or taurine) of C24 bile acids (deconjugated during enterohepatic cycling), conjugation with glucuronate of lipophilic C23-nor bile acids, reduction of oxo groups, and epimerization of iso-(3β-hydroxy) bile acids. Glucose and amino acids enter bile from plasma as secondary solutes and are absorbed efficiently in the biliary ductular system. The biliary system is almost freely permeable to plasma Ca2+; in bile, Ca2+ is bound to bile acid monomers and micelles. Alteration of biliary lipid secretion by orally administered bile acids is a major first step in the medical treatment of calculous biliary disease.