We used a recently developed ELISA format to test the hypothesis that inhibin B is the physiologically active form of inhibin in men. We measured and compared inhibin A, inhibin B, and pro-alpha-C-related immunoreactive peptides (pro-alpha-C-RI) in normal men before and after perturbations of their gonadotropin levels and baseline values in normal men and men with various disturbances of the hypothalamic-pituitary-testicular axis including men with idiopathic hypogonadotropic hypogonadism, infertile men with elevated FSH, men with Klinefelter's syndrome, and orchidectomized men. Mean serum inhibin concentrations were significantly higher in normal men than untreated men with idiopathic hypogonadotropic hypogonadism, infertile men with elevated FSH, untreated men with Klinefelter's syndrome, and orchidectomized men (187 +/- 28 vs 45 +/- 11, 37 +/- 6, 11 +/- 3, and < or = 10 pg/mL, respectively; P < 0.05). Inhibin B levels were below the limit of detection in all of the orchidectomized men. Pro-alpha-C-RI levels were detectable in all men studied including the orchidectomized men, and no significant differences in the pro-alpha-C-RI levels were noted between the normal men and men with various testicular diseases were noted except that orchidectomized men had significantly lower pro-alpha-C-RI levels than all other groups (P < 0.05). Inhibin A was undetectable in all men tested in this study. Six normal men who were administered exogenous levonorgestrel and testosterone had significantly lower serum gonadotropin, inhibin B, and pro-alpha-C-RI levels during the treatment period than the control and recovery periods (P < 0.05). Ten normal men who were administered human recombinant FSH had significantly higher peak serum FSH (21.85 +/- 3.23 IU/L vs. 3.01 +/- 0.51 IU/L), inhibin B (311 +/- 88 pg/mL vs. 151 +/- 23 pg/mL) and pro-alpha-C-RI (646 +/- 69 vs. 402 +/- 38 pg/mL) levels during the treatment period than the baseline values (P < 0.05). We conclude that inhibin B is a unique testicular product that is not detectable in the sera of orchidectomized men, is responsive to FSH stimulation, and has a reciprocal relationship with serum FSH levels in men with various forms of testicular disease. Therefore, inhibin B is likely to be the physiologically important form of inhibin in men.
[1]
A. Mcneilly,et al.
Inhibin-B: a likely candidate for the physiologically important form of inhibin in men.
,
1996,
The Journal of clinical endocrinology and metabolism.
[2]
A. Matsumoto,et al.
Combined administration of levonorgestrel and testosterone induces more rapid and effective suppression of spermatogenesis than testosterone alone: a promising male contraceptive approach.
,
1996,
The Journal of clinical endocrinology and metabolism.
[3]
D. Baird,et al.
Detection of dimeric inhibin throughout the human menstrual cycle by two‐site enzyme immunoassay
,
1994,
Clinical endocrinology.
[4]
N. Groome,et al.
Immunoassays for inhibin and its subunits. Further applications of the synthetic peptide approach.
,
1993,
Journal of immunological methods.
[5]
H. Burger,et al.
Follicle-stimulating hormone is required for quantitatively normal inhibin secretion in men.
,
1988,
The Journal of clinical endocrinology and metabolism.
[6]
H. Burger,et al.
Relative roles of follicle-stimulating hormone and luteinizing hormone in the control of inhibin secretion in normal men.
,
1988,
The Journal of clinical investigation.
[7]
H. Burger,et al.
Inhibin: definition and nomenclature, including related substances.
,
1988,
The Journal of clinical endocrinology and metabolism.