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Do Androgens Directly Regulate Gonadotropin Secretion in the Polycystic Ovary SyndromeÓ^*

DUNAIF ANDREA

Departments of Obstetrics, Gynecology, and Reproductive Science and Medicine, Mt. Sinai School of Medicine, of the City University of New York New York, New York 10029

Address requests for reprints to: Andrea Dunaif, M.D., Departments of Obstetrics, Gynecology, and Reproductive Science and Medicine, Annenberg 20-83, Mt. Sinai School of Medicine, 1 Gustave L. Levy Place, New York, New York 10029.

This study was designed to investigate whether androgens directly, independent of their aromatization to estrogens, distupt gonadotropin secretion in hyperandrogenic women with the polycystic ovary syndrome (PCO). Pulsatile gonadotrpin release and gonadotroph sensitivity to GnRH were deter-mined on consecutive study days basally and during a primed continuous infusion of testosterone (T; n = 4; 100 µg/h;. twice the mean production rate of T in PCO) or dihydrotestosterone (DHT; n = 5; 50 µg/h). To determine if the gonadotropin secretory changes during T infusion were secondary to spontaneous variation, four patients had two consecutive basal studies, and all patients received DHT on the third study day.

T infusion that increased mean plasma T levels from 76 ± 12 (±SE) to 315 ± 28 ng/dl produced no significant changes in the amount or pattern of LH release or in LH sensitivity to GnRH. Mean plasma FSH levels decreased slightly but significantly during T infusion (basal, 242 ± 29 vs. T 226 ± 30 ng/ml LER- 907; P < 0.05 by two-tailed paired t test), but the pulsatile pattern of FSH release and FSH sensitivity to GnRH did not change. DHT infusion increased plasma DHT levels from 17 ± 3 to 244 ± 31 ng/dl, but did not alter the mean levels, pulsatile patterns, or sensitivity to GnRH of LH or FSH. These data suggest that androgens do not directly alter gonadotropin release in PCO. Thus, regulation of the hypothalamic- pituitary axis in women with PCO is different from that in men despite chronic exposure to hyperandrogenemia.

^* This work was supported by the Charles H. Revson Foundation and USPHS Grants K08-HD-00608-01 and RR-00071.

Recipient of a fellowship from the Revson Foundation and of a NICHHD Clinical Investigator Award.

Received October 29, 1985.

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