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The effect of inhibition of cholesterol esterification on the fate of cholesterol derived from HDL in rat hepatocyte monolayers
Author(s) -
Sampson William J.,
Botham Kathleen M.,
Jackson Brian,
Suckling Keith E.
Publication year - 1988
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(88)80893-7
Subject(s) - hepatocyte , intracellular , cholesterol , stimulation , chemistry , monolayer , bile acid , taurocholic acid , hydrolysis , substrate (aquarium) , biochemistry , medicine , endocrinology , biology , in vitro , ecology
Rat HDL 2 is known to stimulate bile acid synthesis in rat hepatocyte monolayers. The intracellular fate of the cholesterol derived from the HDL 2 was studied using the inhibitor of cholesterol esterification, Sandoz compound 58‐035. Rat HDL 2 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 HDL 2 , confirming our earlier observations. 58‐035 prevented this increase. These observations imply that cholesterol entering the cell from HDL 2 is first esterified and can only enter the substrate pool for bile acid synthesis after subsequent intracellular hydrolysis.