This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by MASON, J. I. Articles by RAINEY, W. E. Search for Related Content PubMed PubMed Citation Articles by MASON, J. I. Articles by RAINEY, W. E.

Steroidogenesis in the Human Fetal Adrenal: A Role for Cholesterol Synthesized de Novo^*

Cecil H. and Ida Green Center for Reproductive Biology Sciences and the Departments of Biochemistry and Obstetrics and Gynecology, University of Texas Southwestern Medical School Dallas, Texas 75235

Address all correspondence and requests for reprints to: Dr. J. Ian Mason, Cecil H. and Ida Green Center for Reproductive Sciences, University of Texas Southwestern Medical School, Dallas, Texas 75235.

Primary monolayer cultures of human fetal adrenal cells maintained in either lipoprotein-depleted or lipoprotein-supplemented media responded chronically to ACTH treatment with similarly increased steroid secretion. The principal steroid secreted into each medium was dehydroepiandrosterone sulfate. The presence of human low density lipoprotein (hLDL) in the medium enhanced the secretion of nonsulfoconjugated steroids, especially dehydroepiandrosterone. The secretion rate of 11β-hydroxyandrostenedione was similar to that of cortisol. In the absence of hLDL, ACTH increased cholesterologenesis to maintain the high rates of steroid secretion. After ACTH treatment, increased accumulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase, a rate-determining enzyme of cholesterol biosynthesis, was found. Immunoblot analysis demonstrated that this enzyme was a 97K protein in human fetal adrenal cells. Interestingly, the content of this enzyme in cells treated with ACTH in lipoprotein-depleted medium was similar to that in adrenal fetal zone tissue. This finding suggests that cholester-ologenesis de novo in addition to plasma LDL is important as a source of steroid precursor in vivo in the human fetal adrenal gland.

^* This work was supported in part by NIH Grants 5-P50-HD-11149 and CA-30253, DHHS.

Received June 20, 1986.

This article has been cited by other articles:

				J. Liu, R. Voutilainen, P. Heikkila, and A. I. Kahri Ribonucleic Acid Expression of the CLA-1 Gene, a Human Homolog to Mouse High Density Lipoprotein Receptor SR-BI, in Human Adrenal Tumors and Cultured Adrenal Cells J. Clin. Endocrinol. Metab., August 1, 1997; 82(8): 2522 - 2527. [Abstract] [Full Text] [PDF]