title: Hypogonadotropic hypogonadism as a model of post-natal testicular anti-Müllerian hormone secretion in humans.
abstract: 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. In untreated CHH patients, serum AMH levels were significantly higher than in normal men and similar to those previously reported in prepubertal boys indicating the absence of pubertal maturation of Sertoli cells. In men with AHH, serum AMH levels were also significantly increased when compared to healthy men, but less than in CHH because a persistent testicular T secretion in these patients with less complete gonadotropin deficiency. The high AMH levels in AHH suggest that the post-pubertal suppression of AMH is a reversible phenomenon. In HH patients, hCG treatment induced an increase of plasma T associated with a dramatic decrease of serum AMH, whereas the similar increase in plasma T levels obtained with exogenous T induced only a partial decrease of serum AMH. This dissociation was related to the higher intratesticular T induced by hCG. Taken together, our results confirms the clinical relevance of previous data obtained in rodent models concerning the hormonal regulation of AMH secretion.
authors.affiliation: Service d'Endocrinologie et des Maladies de la Reproduction, Hôpital Bicêtre, 94270 Le Kremlin-Bicêtre, France. jacques.young@bct.ap-hop-paris.fr
authors.forename: Jacques
authors.initials: J
authors.lastname: Young
authors.forename: Rodolfo
authors.initials: R
authors.lastname: Rey
authors.forename: Gilbert
authors.initials: G
authors.lastname: Schaison
authors.forename: Philippe
authors.initials: P
authors.lastname: Chanson
mesh_terms: D000328:Adult; D000818:Animals; D054304:Anti-Mullerian Hormone; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D005640:Follicle Stimulating Hormone / Q000502:physiology; D006023:Glycoproteins / Q000097:blood / Q000378:metabolism* / Q000502:physiology; D006065:Gonadotropins, Pituitary / Q000172:deficiency* / Q000502:physiology; D006801:Humans; D007006:Hypogonadism / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D007985:Leydig Cells / Q000502:physiology; D007986:Luteinizing Hormone / Q000378:metabolism / Q000502:physiology; D008297:Male; D012708:Sertoli Cells / Q000502:physiology; D013735:Testicular Hormones / Q000097:blood / Q000378:metabolism* / Q000502:physiology; D013737:Testis / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D013739:Testosterone / Q000031:analogs & derivatives / Q000097:blood / Q000378:metabolism / Q000494:pharmacology
chemical_list: D006063:Chorionic Gonadotropin; D006023:Glycoproteins; D006065:Gonadotropins, Pituitary; D013735:Testicular Hormones; D013739:Testosterone; C004648:testosterone enanthate; D054304:Anti-Mullerian Hormone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone