Recent evidence suggests that growth hormone (GH) may enhance physiologic p
rocesses, such as spermatogenesis, in addition to causing classical anaboli
c effects. We have previously shown that testosterone restores spermatogene
sis in rats that were made azoospermic by immunization against gonadotropin
-releasing hormone (GnRH). In this study, we investigated whether suppressi
on 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 si
x rats served as controls. Two weeks after the second booster, six rats eac
h 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 rem
aining 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 w
as 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 replenish
ment of germ cells in experimentally induced regressed rat testes.