Human chorionic gonadotropin does not alter patterns of adrenal androgen secretion in primary human adrenal reticularis and fasciculata cell culture.
OBJECTIVE
Controversy surrounds the role of the ovary in maintaining postmenopausal androgen levels. Some postulate that aging ovaries are endocrinologically senescent and that menopausal levels of luteinizing hormone drive the adrenal cortex to secrete increasing amounts of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) as prohormones for subsequent peripheral bioconversion to maintain menopausal testosterone levels. We hypothesized that human chorionic gonadotropin (hCG), acting as an luteinizing hormone analog, would thus augment adrenal androgen secretion from primary human adrenocortical zona reticularis and zona fasciculata cell cultures.


METHODS
Human adrenal glands, obtained from a local organ donation program, were separated microscopically into reticularis and fasciculata zones and were cultured to confluence in serum-supplemented media, followed by a further incubation in defined media. They were then exposed to 24 hours of varying hCG doses, followed by an incubation with defined media and pregnenolone. Supernatants were assayed for adrenal androgens and cortisol. Data were expressed as the molar ratio of (DHEA+ DHEAS)/cortisol and the molar ratio of DHEA/DHEAS. For each of the four runs, mean molar ratios were compared by analysis of variance.


RESULTS
For each of the four runs, the molar ratio was increased 17- to 157-fold in the reticularis compared with the fasciculata cells, indicating efficient zonal separation. Addition of hCG did not alter the molar ratios of adrenal androgens to cortisol or DHEA/DHEAS for either cell type.


CONCLUSIONS
Addition of hCG to human adrenal reticularis or fasciculata cells does not seem to change the pattern of secretion of adrenal androgens or cortisol. It is thus unlikely that luteinizing hormone plays a significant role as an adrenal androgen secretagogue, at least with short-term exposure.
Casson
Peter R
PR
Department of OBGYN, University of Vermont, Burlington 05401, USA. peter.casson@vtmednet.org
Buster
John E
JE
Callas
Peter M
PM
Hornsby
Peter J
PJ
D000302:Adrenal Cortex / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D000728:Androgens / Q000378:metabolism*; D002478:Cells, Cultured / Q000187:drug effects / Q000378:metabolism; D006063:Chorionic Gonadotropin / Q000494:pharmacology*; D003687:Dehydroepiandrosterone / Q000378:metabolism; D019314:Dehydroepiandrosterone Sulfate / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D017698:Postmenopause; D015383:Zona Fasciculata / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D015385:Zona Reticularis / Q000166:cytology / Q000187:drug effects / Q000378:metabolism
D000728:Androgens; D006063:Chorionic Gonadotropin; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate