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1 VA Palo Alto Health Care System, Palo Alto, California, United States; Division of Endocrinology, Stanford University, Stanford, California, United States
2 Division of Endocrinology, Stanford University, Stanford, California, United States
3 Department of Metabolic Disease, University of Tokyo, Tokyo, Japan
4 Department of Internal Medicine, Jichi Medical School, Tochigi, Japan
5 VA Palo Alto Health Care System, Palo Alto, California, United States
* To whom correspondence should be addressed. E-mail: fbk{at}stanford.edu.
Steroid hormones are synthesized using cholesterol as precursor. To determine the functional importance of the LDL receptor and HSL in adrenal steroidogenesis, adrenal cells were isolated from control, HSL-/-, LDLR-/-, and double LDLR/HSL-/- mice. The endocytic and selective uptake of human HDL3-derived cholesteryl esters did not differ among the mice, with selective uptake accounting for >97% of uptake. In contrast, endocytic uptake of either human LDL- or rat HDL-derived cholesteryl esters was reduced 80-85% in LDLR-/- and double LDLR/HSL-/- mice. There were no differences in the selective uptake of either human LDL- or rat HDL-derived cholesteryl esters among the mice. Maximum corticosterone production induced by ACTH or Bt2cAMP and lipoproteins was not altered in LDLR-/- mice, but was reduced 80-90% in HSL-/- mice. Maximum corticosterone production was identical in HSL-/- and double LDLR/HSL-/- mice. These findings suggest that, although the LDL receptor is responsible for endocytic delivery of cholesteryl esters from LDL and rat HDL to mouse adrenal cells, it appears to play a negligible role in the delivery of cholesterol for acute adrenal steroidogenesis in the mouse. In contrast, HSL occupies a vital role in adrenal steroidogenesis because of its link to utilization of selectively delivered cholesteryl esters from lipoproteins.
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