title: Nutritional factors (nutritional aspects) in biliary disorders: bile acid and lipid metabolism in gallstone diseases and pancreaticobiliary maljunction.
abstract: Nutritional factors play a key role in the pathogenesis of biliary diseases such as gallstones and pancreaticobiliary maljunction. Gallstones are primarily classified into cholesterol stone and pigment stone according to the major composition. Cholesterol gallstone formation is very likely based upon supersaturated bile formation, and pigment stones are formed in bile rich in bilirubin. Thus, defects of hepatic metabolism of lipids and organic anions lead to biliary stones. Here, the recent understanding of cholesterol gallstone pathogenesis is elaborated. On the other hand, there is another important link of biliary lipid degradation to serious biliary disease, namely pancreaticobiliary maljunction. Lysophosphatidylcholine (lysoPC), a derivative of phosphatidylcholine hydrolysis by phospholipase A2, is a highly abundant bioactive lipid mediator present in circulation as well as in bile. Increases in bile of lysoPC and phospholipase A2 have been reported in pancreaticobiliary maljunction and considered to be the major risk factor for biliary tract cancers. Further, oxidized fatty acids have been established as a potent ligand for G2A, a member of G protein-coupled receptor family that mediates a diverse array of biological processes including cell growth and apoptosis. Thus, both of lysoPC and free fatty acids are supposed to play an important role through G2A in biliary inflammation and carcinogenesis of pancreaticobiliary maljunction. Taken together, nutritional factors, especially lipid compounds, are seemingly crucial in the pathogenesis of biliary diseases, and such a causal relationship is reviewed by mainly authors' previous publications.
authors.affiliation: Programs of Applied Medicine, Clinical Pharmacotherapy, Department of General Internal Medicine, Hiroshima University Hospital, Graduate School of Medical Science, Hiroshima, Japan.
authors.forename: Susumu
authors.initials: S
authors.lastname: Tazuma
authors.forename: Keishi
authors.initials: K
authors.lastname: Kanno
authors.forename: Akiko
authors.initials: A
authors.lastname: Sugiyama
authors.forename: Nobusuke
authors.initials: N
authors.lastname: Kishikawa
mesh_terms: D000838:Anions / Q000378:metabolism; D001646:Bile / Q000378:metabolism; D001647:Bile Acids and Salts / Q000378:metabolism*; D001652:Bile Ducts / Q000002:abnormalities*; D001661:Biliary Tract Neoplasms / Q000209:etiology; D001663:Bilirubin; D018797:Cell Cycle Proteins / Q000502:physiology; D002784:Cholesterol; D005230:Fatty Acids, Nonesterified / Q000502:physiology; D042882:Gallstones / Q000737:chemistry / Q000145:classification / Q000209:etiology* / Q000378:metabolism*; D006801:Humans; D008024:Ligands; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism; D008244:Lysophosphatidylcholines / Q000378:metabolism; D010084:Oxidation-Reduction; D010183:Pancreatic Ducts / Q000002:abnormalities*; D054467:Phospholipases A2 / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000502:physiology; D012307:Risk Factors
chemical_list: D000838:Anions; D001647:Bile Acids and Salts; D018797:Cell Cycle Proteins; D005230:Fatty Acids, Nonesterified; C115270:G2A receptor; D008024:Ligands; D008244:Lysophosphatidylcholines; D043562:Receptors, G-Protein-Coupled; D002784:Cholesterol; D054467:Phospholipases A2; D001663:Bilirubin
keywords: bile acid metabolism; biliary lipids; biliary physiology