Follicle-stimulating hormone is required for quantitatively normal inhibin secretion in men
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Date
Authors
de Kretser, David M.
Burger, Henry G.
Bremner, William J.
McLachlan, Robert I.
Matsumoto, Alvin M.
Journal Title
Journal ISSN
Volume Title
Publisher
Endocrine Society
Abstract
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 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.
Description
Citation
J Clin Endocrinol Metab. 1988 Dec;67(6):1305-8
