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.

Effect and related mechanism of Yinchenhao decoction on mice with lithogenic diet‑induced cholelithiasis

“…Cholesterol and phospholipids are insoluble in water and must be combined with bile acids to form mixed micelles under normal circumstances (56). When cholesterol is excessively secreted or the excretion of bile salts or phospholipids are reduced, impaired lipid absorption leads to the sustained supersaturation of cholesterol, increasing the susceptibility to cholesterol crystallization and gallstone formation (57,58). Cholesterol supersaturation or deficiency of bile acids in the bile results in a high CSI value, which is a semi-quantitative measure of the biliary cholesterol content (59).…”

Free fatty acids and triglyceride change in the gallbladder bile of gallstone patients with pancreaticobiliary reflux

“…The mechanism of gallstone formation due to PBR is still unclear, and may be related to the hydrolysis of phospholipids and induction of chronic inflammation of gallbladder mucosa. Pancreatic enzymes that are refluxed into the bile duct are easily activated [ 12 , 13 ]. For example, phospholipase A2 (PLA2), which is activated in the biliary tract, hydrolyses phosphatidylcholine (PC), resulting in a lower PC content in the bile [ 6 , 13 ].…”

“…Pancreatic enzymes that are refluxed into the bile duct are easily activated [ 12 , 13 ]. For example, phospholipase A2 (PLA2), which is activated in the biliary tract, hydrolyses phosphatidylcholine (PC), resulting in a lower PC content in the bile [ 6 , 13 ]. Cholesterol, which is slightly soluble in aqueous media, is soluble in bile due to a mixture of bile salts and phospholipids [ 14 ].…”

High Performance Liquid Chromatography-Tandem Mass Spectrometry for the Determination of Bile Acids in Mouse Serum

“…Hepatobiliary and gastrointestinal diseases have been reported to cause changes in bile acid metabolism, while many other diseases might cause changes in bile acid metabolism to different degrees [3][4][5][6][7][8][9][10] . Therefore, it is necessary to establish a simple, rapid and effective bioanalytical method for detecting bile acids in different biological matrices.…”