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Submitted on March 24, 2004
Accepted on November 3, 2004
Service d'Endocrinologie et des Maladies de la Reproduction (J.Y., P.C., S.S., G.S.) and Laboratoire d'Hormonologie (S.B.), Assistance Publique-Hôpitaux de Paris, Bicêtre Hospital and Faculté de médecine Paris XI, 94270 Le Kremlin Bicêtre; Service de Biochimie-Hormonologie, Hôpital Robert Debré, 75019 Paris (M.N.), France; Facultad de Ciencias Biomédicas and Hospital Universitario, Universidad Austral, B1629AJH Pilar, Buenos Aires (M.O'F.), and Centro de Investigaciones Endocrinológicas, Hospital de Niños R. Gutiérrez, C1425EFD Buenos Aires (R.R.), Argentina
* To whom correspondence should be addressed.
Jacques Young, E-mail: jacques.young{at}bct.ap-hop-paris.fr
Serum anti-Müllerian hormone (AMH), a prepubertal Sertoli cell marker, declines during puberty as an early sign of testicular testosterone production. When testosterone synthesis or action is impaired, serum AMH is abnormally high in the first months after birth and at puberty, but normal between these two periods. We postulated that FSH might be responsible for AMH up-regulation in the absence of androgen inhibition.
To test this hypothesis, we administered recombinant human FSH to eight patients aged from 18 to 31 yr with untreated congenital hypogonadotropic hypogonadism. This situation is ideal to study the effect of FSH on AMH production, as it avoids interference by endogenous gonadotropins and testosterone. The patients received daily sc injections of 150 IU rhFSH for one month, followed in seven of them by a combined treatment of rhFSH plus hCG (1500 UI im, twice a week) for two months. Gonadotropins, testosterone, AMH and inhibin B were measured in plasma before treatment, every 10 days during rhFSH treatment and every month during combined rhFSH and hCG treatments.
All hormones were at prepubertal levels before treatment. While LH and testosterone did not vary, AMH and inhibin B levels gradually increased after 20 days of FSH administration. However, in contrast to rhFSH alone, the combined rhFSH plus hCG stimulation of the testis dramatically supress the secretion of AMH and induced a modest but significant reduction of circulating inhibin B levels.
We conclude that FSH stimulates AMH production in the testis when it is at a prepubertal stage. In addition, the decrease of serum AMH during combined rhFSH and hCG testicular stimulation is in agreement with the concept that during pubertal development and in adult life, the suppressive effect of LH-drive testicular androgens outweighs the stimulating effect of FSH on AMH production by Sertoli cells. Finally, the hCG-induced decrease in inhibin B suggest that in humans, as previously demonstrated in monkeys, testicular testosterone is also able to inhibit inhibin B secretion.
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