Growth hormone receptors in the porcine testis during prepuberty.

Supplementation of exogenous growth hormone (GH) during prepuberty advances onset of spermatogenesis in boars, but the mechanism of action is unknown. The present study is an investigation of the presence and characteristics of testicular growth hormone receptors (GHR). A total of 36 boars were castrated, three boars every 10 days, between the ages of 10 and 120 days. Testicular membrane preparations of 10, 20, 30, 50, 70, 100 and 120-day-old boars were used to determine (125)I-bGH binding and Scatchard analysis. Liver from a 60-kg barrow was used for comparison. Specific (125)I-bGH binding to testicular membrane preparations occurred in all age groups with the exception of 20-day-old boars at levels of 30-40% of liver binding. At 30 days of age the unlabelled bGH at 1.1 ng/tube achieved half maximal inhibition (ID(50)). Results of Scatchard analysis indicated a single class of binding sites. Binding affinity was 2.89 x 10(9) m with a binding capacity of 12 fmole/mg membrane protein. The results from this study suggest that GH may act directly on the cells of the prepubertal boar testis.

Diverse testicular responses to exogenous growth hormone and follicle-stimulating hormone in prepubertal boars.

The effects of exogenous growth hormone (GH) and FSH on development of the testes in intact prepubertal boars was investigated. Twenty-four boars received one of four daily treatments from 8 through 40 days of age: 1) 90 micrograms porcine (p) GH/kg body weight (BW), 2) 100 micrograms pFSH/kg BW, 3) GH + FSH, or 4) vehicle only (control). Plasma testosterone levels, measured at 10-day intervals, were similar among groups of boars throughout the study. Body weights among groups were similar during treatment, and testicular weight between treatment groups did not differ at castration (100 days of age). However, total length of the seminiferous tubule per testis in FSH-treated boars was 59% greater than in GH-treated animals (2705 vs. 1704 m; p < 0.05). Diameter of the tubule in GH-treated boars was 58% greater than in FSH-treated boars (p = 0.03). Relative mass of spermatocytes and spermatids in GH-treated animals exceeded that in controls by 2.5-fold and that in FSH boars by 75-fold (p = 0.05). There were no differences in effects of GH + FSH treatment as compared to control treatment; none of the treatments affected any interstitial tissue parameter measured. These results suggest that exogenous FSH had a mitogenic effect on Sertoli cells while delaying tubular maturity, whereas exogenous GH promoted tubular and Sertoli cell maturation, defined as increased Sertoli cell size, lumen formation, and onset of spermatogenesis.