Inhibin B secretion in males with gonadotropin-releasing hormone (GnRH) deficiency before and during long-term GnRH replacement : Relationship to spontaneous puberty, testicular volume, and prior treatment : A clinical research center study

• Published in: The journal of clinical endocrinology and metabolism 1996-10, Vol.81 (10), p.3520-3525
• Main Authors: NACHTIGALL, L. B, BOEPPLE, P. A, SEMINARA, S. B, KHOURY, R. H, SLUSS, P. M, LECAIN, A. E, CROWLEY, W. F
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Biological and medical sciences; Follicle Stimulating Hormone - blood; Gonadotropin-Releasing Hormone - administration & dosage; Gonadotropin-Releasing Hormone - deficiency; Gonadotropin-Releasing Hormone - therapeutic use; Gynecology. Andrology. Obstetrics; Humans; Hypogonadism - drug therapy; Hypogonadism - pathology; Hypogonadism - physiopathology; Inhibins - secretion; Luteinizing Hormone - blood; Male; Male and female genital diseases. Gonadal dysgenesis. Hermaphroditism. Sex hormones resistance; Medical sciences; Periodicity; Puberty - physiology; Testis - pathology; Testosterone - blood
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jc.81.10.3520

To evaluate the physiology of inhibin B in the human male, we measured serum concentrations in normal adult men and men with isolated GnRH deficiency before and during long-term replacement with pulsatile GnRH. At baseline, inhibin B levels in the GnRH-deficient men (n = 31) were significantly lower than normal controls (85 +/- 10 pg/mL vs. 239 +/- 14 pg/mL; P < .01) and correlated positively with pretreatment testicular volume (r = .80, P = .001) and a history of spontaneous puberty, suggesting additional maturational influences on the both testicular volume and inhibin B secretion. Pulsatile GnRH administration was associated with significant increases in inhibin B, with levels averaging 108 +/- 7 pg/mL when serum LH, FSH, and T concentrations had reached the normal adult male range (n = 22; P = .02 vs. baseline). Continued GnRH administration for at least an additional year was not associated with further increases in inhibin B concentrations. Throughout the course of long-term pulsatile GnRH replacement, serum FSH levels were negatively correlated with inhibin B concentrations (e.g. r = -.71, P < 0.01; n = 14 treated 12 months after normalization of T). Although inhibin B concentrations did not correlated with sperm density during therapy, rates of fertility were higher in patients with higher baseline levels (inhibin B > or = 60 pg/mL). Increases in serum concentrations of inhibin B occurring during GnRH replacement demonstrate the gonadotropin regulation of gonadal inhibin B secretion. However, the variation in baseline inhibin B levels before GnRH administration suggests an additional gonadotropin-independent level of modulation. The negative correlation between FSH and inhibin B secretion in GnRH-deficient men receiving long-term GnRH replacement is consistent with a putative role of inhibin B in the negative feedback regulation of FSH, although direct confirmation of this role requires further investigation.