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Endocrinology Section, Gerontology Research, Education, and Clinical Center, Veterans Administration Medical Center; Population Center for Research and Reproduction; and the Divisions of Endocrinology and Gerontology, Department of Medicine, University of Washington School of Medicine Seattle, Washington 98108
The Medical Research Centre, Prince Henry Hospital (H.G.B.), and the Department of Anatomy, Monash University (D.M.d.K.) Melbourne, Australia
Address requests for reprints to: Dr. Robert I. McLachlan, Veterans Administration Medical Center (111), 1660 South Columbian Way, Seattle, Washington 98108.
Inhibin is a glycoprotein hormone produced by the testis and ovary which is postulated to be an important regulator of pituitary FSH secretion. Animal data indicate that inhibin is produced by the Sertoli cells of the testis under the influence of FSH. To determine the role of FSH withdrawal and replacement in the control of inhibin secretion in man, we measured serum inhibin concentrations in men in whom isolated FSH deficiency had been produced by chronic hCG administration; this was followed by FSH replacement. After a 3-month control period, four normal men received hCG for 7 months, resulting in suppression of serum FSH to undetectable levels and urinary FSH excretion to prepubertal levels. Their mean serum inhibin levels fell to 70% of control values during hCG administration [362 ± 60 (±SE) vs. 518 ± 56 U/L; P < 0.01]. While continuing hCG, testosterone enanthate was administered for a further 6 months. Serum FSH and inhibin levels remained suppressed to a similar degree. Testosterone administration then was ceased, and hCG continued for a further 2–4 months. Then, while continuing hCG administration, FSH was replaced as either highly purified human FSH (n = 2) or human menopausal gonadotropin (n = 2) for a period of 4–10 months. Serum FSH levels increased to the mid- and upper normal male ranges, respectively. FSH replacement restored serum inhibin levels to 522 ± 56 U/L (P = NS vs. control). In summary, prolonged selective FSH deficiency induced by chronic hCG administration suppressed inhibin secretion. Replacement of FSH activity restored inhibin secretion to control values. We conclude that 1) FSH is not absolutely required for inhibin secretion in men; and 2) the maintenance of quantitatively normal inhibin secretion requires the combined action of both gonadotropins.
* This work was supported in part by NIH Grant P50-HD-12629, the Australian National Health and Medical Research Council, and the V.A.
Received April 25, 1988.
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