Awoniyi C A, Veeramachaneni D N, Roberts D, Tucker K E, Chandrashekar V, Schlaff W D
Department of Obstetrics and Gynecology, University of Colorado Health Sciences Center, Denver 80262, USA.
J Androl. 1999 Jan-Feb;20(1):102-8.
Recent evidence suggests that growth hormone (GH) may enhance physiologic processes, such as spermatogenesis, in addition to causing classical anabolic effects. We have previously shown that testosterone restores spermatogenesis in rats that were made azoospermic by immunization against gonadotropin-releasing hormone (GnRH). In this study, we investigated whether suppression of GH affects spermatogenesis and the ability of testosterone to restore spermatogenesis following immunization against GnRH and/or growth hormone-releasing hormone (GHRH). Twelve rats were actively immunized against GnRH (anti-GnRH), twelve rats were actively immunized against GHRH (anti-GHRH), six rats were immunized against both GnRH and GHRH (anti-GnRH/GHRH), and six rats served as controls. Two weeks after the second booster, six rats each from the anti-GnRH and anti-GHRH groups as well as the six anti-GnRH/GHRH rats received 24-cm testosterone-filled Silastic implants (T), and the remaining six rats from each of these groups received empty Silastic implants. All rats were euthanized 2 months later. Weights of testes and testicular sperm counts were determined. Serum testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), and insulin-like growth factor-1 (IGF-1) concentrations were determined by radioimmunoassays. Serum GH and IGF-1 were suppressed in anti-GHRH rats. IGF-1 was partially restored by testosterone in anti-GHRH and in anti-GnRH/GHRH rats, but GH was restored to control value in anti-GnRH/GHRH rats. Serum LH and FSH were suppressed in anti-GnRH and anti-GnRH/GHRH rats, but only FSH was partially restored by testosterone. Suppression of GH did not affect maintenance of spermatogenesis. However, because T partially restored GH and IGF-1 levels in anti-GnRH/GHRH rats and because spermatogenesis was found to be restored in these rats, we conclude that GH does not play a role in the maintenance of spermatogenesis in adult rats, but it may be required for the replenishment of germ cells in experimentally induced regressed rat testes.
近期证据表明，生长激素（GH）除了会产生典型的合成代谢作用外，还可能增强生理过程，如精子发生。我们之前已经表明，睾酮可使因免疫促性腺激素释放激素（GnRH）而导致无精子症的大鼠恢复精子发生。在本研究中，我们调查了抑制GH是否会影响精子发生，以及睾酮在免疫GnRH和/或生长激素释放激素（GHRH）后恢复精子发生的能力。12只大鼠主动免疫GnRH（抗GnRH），12只大鼠主动免疫GHRH（抗GHRH），6只大鼠同时免疫GnRH和GHRH（抗GnRH/GHRH），6只大鼠作为对照。第二次加强免疫两周后，抗GnRH组、抗GHRH组的6只大鼠以及6只抗GnRH/GHRH大鼠接受了填充有24厘米睾酮的硅橡胶植入物（T），这些组中其余各6只大鼠接受了空的硅橡胶植入物。2个月后对所有大鼠实施安乐死。测定睾丸重量和睾丸精子计数。通过放射免疫分析法测定血清睾酮、黄体生成素（LH）、卵泡刺激素（FSH）、生长激素（GH）和胰岛素样生长因子-1（IGF-1）浓度。抗GHRH大鼠的血清GH和IGF-1受到抑制。在抗GHRH和抗GnRH/GHRH大鼠中，睾酮可使IGF-1部分恢复，但在抗GnRH/GHRH大鼠中，GH恢复到对照值。抗GnRH和抗GnRH/GHRH大鼠的血清LH和FSH受到抑制，但只有FSH可被睾酮部分恢复。抑制GH并不影响精子发生的维持。然而，由于T可使抗GnRH/GHRH大鼠的GH和IGF-1水平部分恢复，且这些大鼠的精子发生被发现已恢复，我们得出结论，GH在成年大鼠精子发生的维持中不起作用，但在实验诱导的大鼠睾丸退化后生殖细胞的补充中可能是必需的。
