Serum inhibin B levels reflect Sertoli cell function in normal men and men with testicular dysfunction.

Abstract

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.

Prepubertal serum inhibin B in cryptorchid infants and in monorchid boys with compensatory testicular hypertrophy

“…It is produced by the Sertoli cells, partly under the influence of FSH, although other factors might be involved (24). In adult men, a negative feedback between FSH and inhibin B is described and fertile men have significantly higher serum levels of inhibin B and lower FSH levels than infertile men (25,26). In addition, inhibin B levels correlate with testis size and reflect the function of Sertoli cells (27,28).…”

Testicular expression of synaptonemal complex protein 3 (SYCP3) messenger ribonucleic acid in 110 patients with nonobstructive azoospermia

“…Testicular inhibin B regulates the secretion of pituitary FSH. Therefore, elevated serum FSH concentrations in patients with Holstein's scores less than 3 could be due to insufficient inhibin B secretion or immature characteristics of part of the Sertoli cell population (24,26).…”

Impact of Kidney Transplantation on Reproductive Hormone Levels in Males: A Longitudinal Study

“…It regulates FSH secretion by a negative feedback loop to the pituitary gland, and serum levels of inhibin B are positively correlated with testicular volume, sperm concentration, and sperm count [10]. High levels are often seen among normally healthy fertile men while low levels can be a sign of testicular dysfunction [11]. Therefore, levels of inhibin B can serve as a marker of spermatogenesis in men.…”