Open Access
Regulation of the cholesterol ester cycle of cultured Leydig tumor cells
Author(s) -
FREEMAN Dale A.
Publication year - 1987
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1987.tb11065.x
Subject(s) - cholesterol , sterol o acyltransferase , chemistry , steroid , hydrolysis , steroid hormone , hormone , reverse cholesterol transport , medicine , endocrinology , biochemistry , lipoprotein , biology
The MA‐10 Leydig tumor cells take up low‐density lipoprotein (LDL) from the medium and store the LDL‐derived cholesterol as cholesterol esters that can be subsequently mobilized and used for steroid hormone synthesis. The present studies investigate the mechanisms by which cAMP acutely regulates the cellular content of cholesterol esters. In the absence of cholesterol utilization for steroidogenesis, cAMP stimulates cholesterol ester hydrolysis and ester resynthesis proportionally. The augmentation of ester hydrolysis by cAMP is completely matched by increased activity of the acyl‐coenzyme‐A: cholesterol acyltransferase and thus does not regulate cellular cholesterol ester concentration per se. The more important action of cAMP is to interrupt the cycle of hydrolysis and ester resynthesis by decreasing cholesterol re‐esterificaton. In cells activity synthesizing steroid hormones, cholesterol reesterification is decreased by 82%. The decrease in cholesterol re‐esterification occurs because cAMP directs cholesterol normally destined for re‐esterification into steroid synthesis; simply blocking the utilization of cholesterol for steroidogenesis completely prevents net cholesterol ester hydrolysis and increases the cellular rate of cholesterol esterification.