Castration and testosterone effects on endogenous and somatocrinin-induced growth hormone release in intact and castrated male pigs.

Growth hormone (GH) release is influenced mainly by two hypothalamic factors, growth hormone-releasing factor (GRF) and somatostatin and is modulated by other hormones such as gonadal steroids. The objective of this study was to determine if castration (CA) and exogenous testosterone (TE) affect endogenous and GRF-induced GH release. Purebred Yorkshire male pigs (n = 32) were assigned to one of the following treatments: T1:CA; T2:CA +/- TE; T3: intact (IN); T4: IN +/- TE, in a 2 x 2 factorial design. Piglets were castrated at 3 days of age. Testosterone propionate (1.0 mg/kg) in sesame oil (2 ml) or sesame oil alone was injected sc SID during a 10-day period before each sampling day at 9, 15 and 21 weeks of age. Jugular blood samples were collected for a 6-hr period preceding and following iv injection of hGRF (1-29)NH2 (10 micrograms/kg). These procedures were repeated at 9, 15 and 21 weeks of age. The overall mean GH levels and the area under the GH peaks before and after GRF stimulation were lower (P less than .05) in castrated animals than in intact animals. Testosterone treatment increased (P less than .05) circulating TE levels and increased the amplitude of the endogenous GH peaks but did not affect (P greater than .05) the GRF-induced GH release. Increasing age produced a marked reduction of the amplitude of the GH peaks, the area under the GH peaks, the baseline mean and the overall mean GH levels during the 6-hr period preceding GRF injection. The present data support the hypothesis that castration in pigs reduces circulating and GRF-induced GH release. Exogenous testosterone for 10 days did not stimulate endogenous or GRF-induced GH release with the exception of the amplitude of the endogenous GH peaks.