Hormone receptors in livers of GH3 tumor-bearing rats: the predominant effect of growth hormone and testosterone

Abstract

The relationship between serum levels of rat GH (rGH), rat PRL (rPRL), corticosterone, estrogen, and testosterone and the liver-binding sites specific to [125I]iodo-human GH (hGH), -human PRL (hPRL), and -rPRL were investigated in normal rats, in rats bearing the GH- and PRL-secreting tumor (GH3), and in rats 14 days after tumor removal. The GH3 tumor elevated serum levels of rGH and rPRL and concomitantly increased the hepatic binding of radioiodinated hGH, hPRL, and rPRL; male rats had a greater increase than female rats. The increased binding was due to an increase in the specific membrane-binding sites, the receptors, whereas the affinity constant of binding (Ka) was not altered. In both male and female rats, the specific binding of receptors and the total binding capacities of livers correlated positively with serum levels of rGH (P less than 0.02) and inversely with serum levels of testosterone (P less than 0.05). There was insignificant or no correlation between rPRL or other steroids and the total liver-binding capacities. These results suggested that GH was the primary inducer and testosterone was the predominant regulator of the hepatic receptors in rats. The observed sex difference in the increase of receptors by GH3 tumor indicated that in normal and tumor-removed male rats, testosterone had suppressed the induction of hepatic receptors.