title: Inhibin B in males with gonadotropin-releasing hormone (GnRH) deficiency: changes in serum concentration after shortterm physiologic GnRH replacement--a clinical research center study.
abstract: To examine the role of inhibin B in the feedback regulation of FSH secretion in the human male, we determined serial levels in 18 men with idiopathic hypogonadotropic hypogonadism (IHH) during their initial 8 weeks of GnRH replacement. Pulsatile GnRH was administered every 2 h, with the dose increased at 2-week intervals (5-50 ng/kg/bolus). Every 2 weeks, sera were assayed for inhibin B, FSH, LH, and testosterone. Serial comparisons were performed within the IHH group as well as vs. normal men (n = 20). The baseline inhibin B level in IHH patients averaged 68 +/- 11 pg/mL (mean +/- SEM), significantly less than that in normal men (239 +/- 14 pg/mL; P < 0.001). After 8 weeks of pulsatile GnRH, inhibin B levels in the IHH patients increased significantly to 118 +/- 14 pg/mL (P = 0.003). During GnRH replacement, FSH concentrations correlated negatively with inhibin B concentrations at all doses. Patients previously treated with testosterone began with somewhat lower inhibin B levels but demonstrated a significantly greater increase in serum concentrations than patients who had received prior gonadotropin or GnRH therapy. A history of cryptorchidism did not have a significant impact on inhibin B concentrations before or during GnRH replacement. The low inhibin B levels in IHH men at baseline and their prompt increase in response to pulsatile GnRH suggest acute regulation by gonadotropin stimulation of the testis. The variation in inhibin B levels at baseline and in response to GnRH suggest that prior gonadotropin exposure and seminiferous tubular development also modulate inhibin B secretion. The consistent negative correlation between FSH and inhibin B during the induction of sexual maturation with GnRH supports the role of gonadal inhibin B secretion as an important endocrine regulator of FSH in the human male.
authors.affiliation: Reproductive Endocrine Unit, Massachusetts General Hospital, Boston 02114, USA.
authors.forename: S B
authors.initials: SB
authors.lastname: Seminara
authors.forename: P A
authors.initials: PA
authors.lastname: Boepple
authors.forename: L B
authors.initials: LB
authors.lastname: Nachtigall
authors.forename: F P
authors.initials: FP
authors.lastname: Pralong
authors.forename: R H
authors.initials: RH
authors.lastname: Khoury
authors.forename: P M
authors.initials: PM
authors.lastname: Sluss
authors.forename: A E
authors.initials: AE
authors.lastname: Lecain
authors.forename: W F
authors.initials: WF
authors.lastname: Crowley
mesh_terms: D000293:Adolescent; D000328:Adult; D003456:Cryptorchidism / Q000097:blood; D005246:Feedback; D005640:Follicle Stimulating Hormone / Q000097:blood / Q000378:metabolism; D007987:Gonadotropin-Releasing Hormone / Q000008:administration & dosage / Q000172:deficiency* / Q000627:therapeutic use*; D006801:Humans; D007006:Hypogonadism / Q000097:blood / Q000188:drug therapy*; D007265:Inhibins / Q000097:blood*; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D010507:Periodicity; D012016:Reference Values; D013739:Testosterone / Q000097:blood
chemical_list: D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D007265:Inhibins; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone