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dc.contributor.authorde Kretser, David M.en_US
dc.contributor.authorBurger, Henry G.en_US
dc.contributor.authorBremner, William J.en_US
dc.contributor.authorMcLachlan, Robert I.en_US
dc.contributor.authorMatsumoto, Alvin M.en_US
dc.date.accessioned2008-10-17T20:42:16Z
dc.date.available2008-10-17T20:42:16Z
dc.date.issued1988-12en_US
dc.identifier.citationJ Clin Endocrinol Metab. 1988 Dec;67(6):1305-8en_US
dc.identifier.urihttp://hdl.handle.net/1773/4408
dc.description.abstractInhibin 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 less than 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.en_US
dc.language.isoen_USen_US
dc.publisherEndocrine Societyen_US
dc.subjectmale contraceptionen_US
dc.subjectandrologyen_US
dc.subjectgonadotropinsen_US
dc.subject5-alpha reductase inhibitorsen_US
dc.subjectspermatogenesisen_US
dc.subjecttestosteroneen_US
dc.subjectcolchicineen_US
dc.subjectklinefelter's syndromeen_US
dc.subjectreifenstein's syndromeen_US
dc.subject.meshFollicle Stimulating Hormone, deficiency, pharmacology, physiologyen_US
dc.subject.meshDrug Interactionsen_US
dc.subject.meshMaleen_US
dc.subject.meshResearch Support, U.S. Gov't, Non-P.H.S.en_US
dc.subject.meshInhibins, blood, secretionen_US
dc.subject.meshResearch Support, U.S. Gov't, P.H.S.en_US
dc.subject.meshSperm Count, drug effectsen_US
dc.subject.meshResearch Support, Non-U.S. Gov'ten_US
dc.subject.meshAdulten_US
dc.subject.meshChorionic Gonadotropin, pharmacologyen_US
dc.subject.meshTestosterone, analogs & derivatives, pharmacologyen_US
dc.titleFollicle-stimulating hormone is required for quantitatively normal inhibin secretion in menen_US
dc.typeArticleen_US


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