Bremner W J, Matsumoto A M, Sussman A M, Paulsen C A
J Clin Invest. 1981 Oct;68(4):1044-52. doi: 10.1172/jci110327.
The role of follicle-stimulating hormone (FSH) in the control of spermatogenesis is not well established in any species, including man. We studied the effect of an experimentally-induced, selective FSH deficiency on sperm production in normal men. After a 3-mo control period, five normal men received testosterone enanthate (T) 200 mg i. m. weekly to suppress luteinizing hormone (LH) and FSH, until three successive sperm counts revealed azoospermia or severe oligospermia (sperm counts <3 million/ml). Then, while continuing T, human chorionic gonadotropin (hCG) 5,000 IU i. m. three times weekly was administered simultaneously to replace LH activity, leaving FSH activity suppressed. The effect of the selective FSH deficiency produced by hCG plus T administration on sperm production was determined. Sperm counts (performed twice monthly throughout the study) were markedly suppressed during T administration alone (1.0+/-1.0 million/ml mean+/-SE, compared with 106+/-28 million/ml during the control period, P < 0.001). With the addition of hCG to T, sperm counts returned toward normal (46+/-16 million/ml, P < 0.001 compared with T alone). In two subjects, sperm counts during hCG plus T returned into the individual's control range. Sperm motility and morphology were consistently normal in all men during hCG plus T. Serum FSH levels by RIA were normal (110+/-10 ng/ml) in the control period and were suppressed to undetectable levels (<25 ng/ml) in the T alone and hCG plus T periods. Urinary FSH excretion was markedly suppressed in the T alone (60+/-15 mIU/h-2nd IRP, P < 0.01) and hCG plus T (37+/-9 mIU/h, P < 0.01) periods compared with the control period (334+/-78 mIU/h). We conclude that spermatogenesis as assessed by sperm counts, motilities, and morphologies may be reinitiated and maintained at normal levels in men with undetectable blood FSH levels and urinary excretion of FSH less than that of prepubertal children. This conclusion implies that, although FSH may exert effects on human testicular function, maintenance of normal spermatogenesis and reinitiation of sperm production after short-term suppression by exogenous steroids can occur in spite of nearly absent FSH stimulation.
促卵泡激素(FSH)在包括人类在内的任何物种的精子发生控制中的作用尚未完全明确。我们研究了实验诱导的选择性FSH缺乏对正常男性精子生成的影响。在为期3个月的对照期后,5名正常男性每周肌肉注射200mg庚酸睾酮(T)以抑制黄体生成素(LH)和FSH,直到连续三次精子计数显示无精子症或严重少精子症(精子计数<300万/ml)。然后,在继续使用T的同时,每周三次肌肉注射5000IU人绒毛膜促性腺激素(hCG)以替代LH活性,而FSH活性仍被抑制。确定了hCG加T给药产生的选择性FSH缺乏对精子生成的影响。在整个研究过程中每月进行两次精子计数,单独使用T期间精子计数显著降低(平均±标准误为1.0±1.0万/ml,而对照期为106±28万/ml,P<0.001)。在T中加入hCG后,精子计数恢复正常(46±16万/ml,与单独使用T相比P<0.001)。在两名受试者中,hCG加T期间的精子计数恢复到个体的对照范围内。在hCG加T期间,所有男性的精子活力和形态始终正常。放射免疫分析法测定的血清FSH水平在对照期正常(110±10ng/ml),在单独使用T期和hCG加T期被抑制到无法检测的水平(<25ng/ml)。与对照期(334±78mIU/h)相比,单独使用T期(60±15mIU/h - 第二国际参考品,P<0.01)和hCG加T期(37±9mIU/h,P<0.01)的尿FSH排泄显著降低。我们得出结论,对于血FSH水平无法检测且尿FSH排泄低于青春期前儿童的男性,可以通过精子计数、活力和形态评估重新启动精子发生并维持在正常水平。这一结论意味着,尽管FSH可能对人类睾丸功能有影响,但尽管几乎没有FSH刺激,在短期受到外源性类固醇抑制后,仍可维持正常精子发生并重新启动精子生成。