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The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 2 860-866
Copyright © 2004 by The Endocrine Society

Administration of Dihydrotestosterone to Rhesus Monkeys Inhibits Gonadotropin-Stimulated Ovarian Steroidogenesis

Anthony J. Zeleznik, Lynda Little-Ihrig and Suresh Ramasawamy

Department of Physiology and Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261

Address all correspondence and requests for reprints to: Anthony J. Zeleznik, Ph.D., 830 Scaife Hall, University of Pittsburgh School of Medicine, 3550 Terrace Street, Pittsburgh, Pennsylvania 15261. E-mail: zeleznik{at}pitt.edu.

Androgens, in addition to serving as a substrate for estrogen biosynthesis, exert autocrine/paracrine actions on ovarian function. However, much of the information regarding the actions of androgens on the ovary has been obtained using rodents, and the extent to which these results can be extrapolated to higher primates is uncertain. The current study was initiated to determine the effects of dihydrotestosterone (DHT) and testosterone (T) on the responsiveness of the rhesus monkey ovary to exogenous FSH and LH in vivo. Rhesus monkeys whose spontaneous gonadotropin secretion was interrupted with a GnRH antagonist received sc implants of either DHT or T for 5 d before and continuing throughout a 15-d iv infusion of human FSH and LH. Neither T nor DHT treatment synergized with FSH/LH to stimulate estrogen production or increases in ovarian weight. Rather, administration of DHT significantly reduced estrogen secretion and the augmentation of ovarian weight in response to exogenously administered FSH and LH. These results indicate that high concentrations of DHT are antagonistic to gonadotropin-stimulated ovarian function in primates.

This work was supported by the NICHHD, NIH, through cooperative agreement U54-HD-08610 as part of the Specialized Cooperative Centers Program in Reproduction Research.

Abbreviations: DHT, Dihydrotestosterone; h, human; hCG, human chorionic gonadotropin; PCOS, polycystic ovarian syndrome; T, testosterone.




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