SERUM INHIBIN-B LEVELS REFLECT SERTOLI-CELL FUNCTION IN NORMAL MEN AND MEN WITH TESTICULAR DYSFUNCTION

We used a recently developed ELISA format to test the hypothesis that inhibin B is the physiologically active form of inhibin in men. We mea sured and compared inhibin A, inhibin B, and pro-alpha-C-related immun oreactive peptides (pro-alpha-C-RI) in normal men before and after per turbations of their gonadotropin levels and baseline values in normal men and men with various disturbances of the hypothalamic-pituitary-te sticular axis including men with idiopathic hypogonadotropic hypogonad ism, infertile men with elevated FSH, men with Klinefelter's syndrome, and orchidectomized men. Mean serum inhibin concentrations were signi ficantly higher in normal men than untreated men with idiopathic hypog onadotropic hypogonadism, infertile men with elevated FSH, untreated m en with Klinefelter's syndrome, and orchidectomized men (187 +/- 28 vs . 45 +/- 11, 37 +/- 6, 11 +/- 3, and less than or equal to 10 pg/mL, r espectively; P < 0.05). Inhibin B levels were below the limit of detec tion in all of the orchidectomized men. Pro-alpha-C-RI levels were det ectable in all men studied including the orchidectomized men, and no s ignificant differences in the pro(U-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 level s than all other groups (P < 0.05). Inhibin A was undetectable in all men tested in this study. Six normal men who were administered exogeno us levonorgestrel and testosterone had significantly lower serum gonad otropin, inhibin B, and pro-alpha-C-RI levels during the treatment per iod than the control and recovery periods (P < 0.05). Ten normal men w ho were administered human recombinant FSH had significantly higher pe ak serum FSH (21.85 +/- 3.23 IU/L us. 3.01 +/- 0.51 IU/L), inhibin B ( 311 +/- 88 pg/mL us. 151 +/- 23 pg/mL) and pro-alpha-C-RI (646 +/- 69 us. 402 +/- 38 pg/mL) levels during the treatment period than the base line values (P < 0.05). We conclude that inhibin B is a unique testicu lar product that is not detectable in the sera of orchidectomized men, is responsive to FSH stimulation, and has a reciprocal relationship w ith serum FSH levels in men with various forms of testicular disease. Therefore, inhibin B is likely to be the physiologically important for m of inhibin in men.