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Stimulation of Serum Inhibin Concentrations by Gonadotropin-Releasing Hormone in Men With Idiopathic Hypogonadotropic Hypogonadism^*

Medical Service and Gerontology Research, Education, and Clinical Center, Veterans Administration Medical Center Seattle, Washington 98108
Population Center for Research in Reproduction Seattle, Washington 98108
the Divisions of Endocrinology and Gerontology, Department of Medicine, University of Washington School of Medicine Seattle, Washington 98108
the Medical Research Centre, Prince Henry’s Hospital (H.G.B.), and the Department of Anatomy, Monash University (D.M.d.K.) Melbourne, Australia 3168

Address requests for reprints to: William J. Bremner, M.D., Ph.D., Veterans Administration Medical Center (111), 1660 South Columbian Way, Seattle, Washington 98108.

Inhibin is a gonadal hormone thought to be important in FSH regulation. We investigated the effects of the hypogonadotropic state and subsequent GnRH-induced increases in gonadotropin levels on inhibin secretion. Serum levels of inhibin, LH, FSH, and testosterone (T) as well as sperm concentrations were measured in 5 men with idiopathic hypogonadotropic hypogonadism (IHH) before (baseline) and during 8 weeks of GnRH therapy (5 µg, sc, every 2 h). Baseline and peak inhibin levels were compared to those in a group of 19 normal men. Before GnRH administration, the mean serum inhibin level was significantly lower in the IHH men than in the normal men [166 ± 56 (±SE) vs. 588 ± 30 U/L; P < 0.001]. Serum inhibin levels rose after 1 week of GnRH therapy (P < 0.05) and remained higher than the baseline level thereafter. The mean peak inhibin level during GnRH administration was lower than the mean value in normal men (485 ± 166 vs. 588 ± 30 U/L; P < 0.05). Serum LH and FSH levels rose promptly to the midnormal range or slightly above it. Serum T levels did not significantly increase until 4–5 weeks of GnRH administration and remained in the low normal range. All IHH men were azoospermic throughout the study. These data are consistent with the hypothesis that inhibin is produced by the testis under gonadotropin control. They also suggest the possibility of defective Sertoli and Leydig cell function in men with IHH, since the men’s serum inhibin and T levels did not rise to the same extent as did their normalized serum gonadotropin levels during GnRH administration.

^* This work was supported in part by NIH Grant P-50-HD-12629, the V.A., the Australian National Health and Medical Research Council, and the Clinical Research Center at the University of Washington, supported by NIH Grant RR-37.

Received April 19, 1988.