Suppression of growth hormone does not affect ongoing spermatogenesis in rats.
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.
Awoniyi
C A
CA
Department of Obstetrics and Gynecology, University of Colorado Health Sciences Center, Denver 80262, USA. caleb.awoniyi@uchsc.edu
Veeramachaneni
D N
DN
Roberts
D
D
Tucker
K E
KE
Chandrashekar
V
V
Schlaff
W D
WD
D000818:Animals; D001835:Body Weight; D005640:Follicle Stimulating Hormone / Q000097:blood; D013006:Growth Hormone / Q000037:antagonists & inhibitors* / Q000097:blood / Q000276:immunology; D013007:Growth Hormone-Releasing Hormone / Q000276:immunology; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D013091:Spermatogenesis / Q000187:drug effects*; D013737:Testis / Q000166:cytology; D013739:Testosterone / Q000097:blood / Q000494:pharmacology*
D013739:Testosterone; D007334:Insulin-Like Growth Factor I; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone