title: Interrelationships of bile acid and phospholipid fatty acid species with cholesterol saturation of duodenal bile in health and gallstone disease.
abstract: The relative amount of cholesterol and the fatty acid composition of phosphatidylcholines in bile can be influenced by the bile acid species secreted. To search for a contribution of secondary bile acids and of phosphatidylcholines to supersaturation of bile in gallstone disease, we compared the relative amount of cholesterol and the biliary composition of bile acids and of phospholipid fatty acids in cholecystokinin-stimulated duodenal bile of 22 female gallstone patients and 16 healthy controls and analyzed the interrelationships of these bile constituents. Gallstone patients had higher molar percentages of cholesterol than did controls (10.2 +/- 3.2 vs. 6 +/- 1.5 mol%; p less than 0.001) and demonstrated a trend toward larger fractions of deoxycholic and lithocholic acids. By linear models, variation of cholesterol saturation could be predicted (p less than 0.001) up to 53% by the bile acid pattern and up to 81% by the fatty acid pattern of phospholipids. Linear path analysis (goodness-of-fit index = 0.973) confirmed the tight relationship between phospholipid fatty acids (positive: oleic, arachidonic; negative: linoleic, palmitoleic) and the relative amount of cholesterol; more than half the influence of cholic, deoxycholic and lithocholic acids on the relative amount of cholesterol could be explained indirectly by their influence on the phospholipid fatty acid pattern. We conclude that the relationships examined by path analysis support the working hypothesis that secondary bile acids contribute to supersaturation of bile mainly by changing the fatty acid pattern of the secreted phospholipids (presumably the pattern of phosphatidylcholines), which increases the molar ratio of cholesterol/phospholipids in bile.
authors.affiliation: Department of Medicine II, University of Munich, Germany.
authors.forename: F
authors.initials: F
authors.lastname: Berr
authors.forename: E
authors.initials: E
authors.lastname: Schreiber
authors.forename: U
authors.initials: U
authors.lastname: Frick
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001646:Bile / Q000187:drug effects / Q000378:metabolism*; D001647:Bile Acids and Salts / Q000378:metabolism*; D002766:Cholecystokinin / Q000494:pharmacology; D002769:Cholelithiasis / Q000503:physiopathology* / Q000628:therapy; D002784:Cholesterol / Q000378:metabolism*; D005227:Fatty Acids / Q000032:analysis*; D005260:Female; D005704:Gallbladder / Q000502:physiology / Q000503:physiopathology*; D006801:Humans; D008096:Lithotripsy; D008954:Models, Biological; D010743:Phospholipids / Q000378:metabolism*; D012016:Reference Values
chemical_list: D001647:Bile Acids and Salts; D005227:Fatty Acids; D010743:Phospholipids; D002766:Cholecystokinin; D002784:Cholesterol