Human Reproduction, Vol. 18, No. 4, 734-743,
April 2003
© 2003 European Society of Human Reproduction and Embryology
Response of serum inhibin B and pro-
C levels to gonadotrophic stimulation in normal men before and after steroidal contraceptive treatment
1 Prince Henry’s Institute of Medical Research, Monash Medical Centre and 2 Department of Obstetrics and Gynaecology, Monash University, Clayton, Victoria 3168, Australia
3 To whom correspondence should be addressed at: Prince Henry’s Institute of Medical Research, PO Box 5152, Clayton, Victoria 3168, Australia. e-mail: rob.mclachlan{at}med.monash.edu.au
BACKGROUND: Testicular regulation of inhibin B may be influenced by the germ cell complement. METHODS: We examined the effects of gonadotrophin stimulation on serum inhibin B and pro-
C in 25 normal men at (i) control (stimulation test 1), (ii) after spermatogenic suppression induced by testosterone plus progestin treatment (stimulation test 2), and (iii) during spermatogenic recovery induced by FSH and/or hCG treatment (stimulation test 3). For each test, subjects received a single injection of 1200 IU FSH or 5000 IU hCG or both. RESULTS: Inhibin B and pro-C fell with spermatogenic suppression (75 and 51% of pre-treatment baseline respectively, P < 0.05). Inhibin B response to FSH (130–144%) was similar in controls and after germ cell suppression. Pro-C response after germ cell suppression compared with control was significantly increased (P < 0.05) with both FSH (210–229% versus 140–185%) and hCG (254–261% versus 145%). All treatments partially restored spermatogenesis with no clear relationship apparent between inhibin B and sperm count. CONCLUSIONS: We conclude that: (i) serum inhibin B and pro-C are only partially gonadotrophin dependent, (ii) spermatogenic suppression does not modify inhibin B response to FSH but enhances pro-C response to both FSH and hCG, and (iii) inhibin B is a poor marker of spermatogenesis in this model of gonadotrophic manipulation in normal men.
Key words: FSH/inhibin/LH/Sertoli cell/testosterone
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