Testicular anti-mullerian hormone secretion is stimulated by recombinant human FSH in patients with congenital hypogonadotropic hypogonadism.

Serum anti-Mullerian hormone (AMH), a prepubertal Sertoli cell marker, declines during puberty as an early sign of testicular testosterone (T) production. When T 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.

Hypogonadotropic hypogonadism as a model of post-natal testicular anti-Müllerian hormone secretion in humans.

The pituitary gonadotropins are the main regulators of testicular hormonal secretion in humans. Hypogonadotropic hypogonadism (HH), characterized by the absence of secretion of endogenous gonadotropins is therefore a convenient model to asses the respective effects of luteinizing hormone (LH) (or human chorionic gonadotropin (hCG)), exogenous testosterone (T) and FSH on gonadal function. In order to investigate the hormonal control of AMH secretion in man, serum AMH levels were measured in adult patients with congenital HH (CHH) and with post-pubertal acquired HH (AHH) either untreated, during hCG or T therapy.