Gonadal steroids influence serum somatomedin-C concentrations in prepubertal female rhesus monkey.

Abstract

The present study examined the influence of estradiol (E2) and androstenedione (delta 4) on the regulation of GH and somatomedin-C (Sm-C) secretion in prepubertal female rhesus monkeys. Ovariectomized animals (n = 9) received empty capsules (0) or capsules filled with E2 or delta 4 in successive 2-week treatment blocks as follows: 0, E2, E2 plus delta 4, 0, delta 4, delta 4 plus E2, and 0. Serum samples were collected twice weekly for determination of basal hormone levels. Implantation of delta 4 capsules elevated serum delta 4 and testosterone concentrations, but did not influence E2 levels. Conversely, treatment with E2 only elevated serum E2. Basal concentrations of serum GH were unaffected by steroid treatment as levels varied between 5.5 and 9.5 ng/ml during the study. In contrast, Sm-C concentrations were increased significantly by each steroid treatment. Levels of Sm-C were elevated by delta 4 treatment (450.7 +/- 33.2 ng/ml) compared to baseline (376.2 +/- 37.7 ng/ml), whereas concentrations were maximally increased by E2 administration (greater than 600 ng/ml). The addition of delta 4 to the E2 treatment regimen did not further increase Sm-C levels. Regression analyses revealed that neither delta 4 nor testosterone concentrations were related to Sm-C or GH levels. In contrast, levels of E2 (r = 0.81) and GH (r = 0.42), which were not related to one another, were significantly correlated with Sm-C concentrations. Indeed, the multiple regression of E2 and GH on Sm-C accounted for significantly more variance in Sm-C levels (R2 = 0.706) than either hormone alone. These data suggest that E2 is responsible for the steroid-induced increases in Sm-C secretion observed previously in prepubertal females. Since steroid treatment elevated Sm-C levels independent of consistent changes in basal GH secretion, the effect is probably the result of either a direct E2 action on Sm-C release in the presence of a normal GH secretory pattern or an exacerbation of the nocturnal secretion of GH.