title: The effect of inhibition of cholesterol esterification on the fate of cholesterol derived from HDL in rat hepatocyte monolayers.
abstract: Rat HDL2 is known to stimulate bile acid synthesis in rat hepatocyte monolayers. The intracellular fate of the cholesterol derived from the HDL2 was studied using the inhibitor of cholesterol esterification, Sandoz compound 58-035. Rat HDL2 added to rat hepatocyte monolayers caused a stimulation of cholesterol esterification of 32%. This stimulation could be inhibited by 58-035. A small significant increase in bile acid synthesis was also observed in cells in the presence of HDL2, confirming our earlier observations. 58-035 prevented this increase. These observations imply that cholesterol entering the cell from HDL2 is first esterified and can only enter the substrate pool for bile acid synthesis after subsequent intracellular hydrolysis.
authors.affiliation: Department of Cellular Pharmacology, Smith Kline & French Research Ltd, Welwyn, England.
authors.forename: W J
authors.initials: WJ
authors.lastname: Sampson
authors.forename: K M
authors.initials: KM
authors.lastname: Botham
authors.forename: B
authors.initials: B
authors.lastname: Jackson
authors.forename: K E
authors.initials: KE
authors.lastname: Suckling
mesh_terms: D000577:Amides / Q000494:pharmacology*; D000818:Animals; D001647:Bile Acids and Salts / Q000096:biosynthesis; D002478:Cells, Cultured; D002788:Cholesterol Esters / Q000096:biosynthesis; D008076:Cholesterol, HDL / Q000378:metabolism*; D007700:Kinetics; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D017646:Organosilicon Compounds; D051381:Rats; D002785:Sterol O-Acyltransferase / Q000037:antagonists & inhibitors*
chemical_list: D000577:Amides; D001647:Bile Acids and Salts; D002788:Cholesterol Esters; D008076:Cholesterol, HDL; D017646:Organosilicon Compounds; C040256:SAN 58035; D002785:Sterol O-Acyltransferase