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Submitted on May 14, 2003
Accepted on November 10, 2003
1 VA Palo Alto Health Care System, Palo Alto, CA 94304, Department of Medicine, Stanford University, Stanford, CA 94305, Department of Metabolic Disease, University of Tokyo, Tokyo 113, Japan, Department of Internal Medicine, Jichi Medical School, Tochigi, Japan
* To whom correspondence should be addressed. E-mail: fbk{at}stanford.edu.
Steroid hormones are synthesized using cholesterol as precursor, with a substantial portion supplied by the selective uptake of lipoprotein-derived cholesteryl esters. Adrenals express a high level of neutral cholesteryl ester hydrolase (CEH) activity, and recently hormone-sensitive lipase (HSL) was shown to be responsible for most adrenal neutral CEH activity. To determine the functional importance of HSL in adrenal steroidogenesis, adrenal cells were isolated from control and HSL-/- mice and the in vitro production of corticosterone was quantified. Results show that, even though adrenal cholesteryl ester content was substantially elevated in both male and female HSL-/- mice, basal corticosterone production was reduced 
50%. The maximum corticosterone production induced by Bt2cAMP and lipoproteins was 75-85% lower in adrenal cells from HSL-/- mice compared with control. There is no intrinsic defect in the conversion of cholesterol into steroids in HSL-/- mice. Bt2cAMP-stimulated conversion of HDL cholesteryl esters into corticosterone was reduced 97% in HSL-/- mice. An increase in LDL receptor expression appears to be one of the compensatory mechanisms for cholesterol delivery in HSL-/- mice. These findings suggest that HSL is functionally linked to the selective pathway and is critically involved in the intracellular processing and availability of cholesterol for adrenal steroidogenesis.
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