Induction of Hepatic Receptors for Growth Hormone (GH) and Prolactin by GH Infusion Is Sex Independent*

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Abstract
To determine whether induction of rat liver GH [growth hormone] and PRL [prolactin] receptors by GH infusion is dependent upon the sex of the animal or whether or not the pituitary is intact, rat GH (rGH) or rat PRL (rPRL) was infused at .apprx. 200 .mu.g/day for 7 days into male and female, intact and hypophysectomized rats, and the binding of radioiodinated bovine GH (bGH) and ovine PRL (oPRL) to liver microsomal membranes was measured. In females, bGH binding was reduced by hypophysectomy whether or not membranes were MgCl2 treated to remove endogenous ligand. In males, hypophysectomy caused an apparent 3-fold induction of bGH binding sites, which was absent in MgCl2-treated membranes, suggesting that the effect was due to receptor occupancy by endogenous rGH in the intact males. Hypophysectomy also lowered oPRL binding in females but had no effect in males. Infusion of rGH significantly induced binding sites for bGH and oPRL in all treatment groups, independently of sex or the presence of the pituitary, whereas rPRL infusion had no effect on either receptor type except for mild induction of bGH binding in hypophysectomized females. Serum somatomedin-C (SM-C), reduced 95% by hypophysectomy, was restored by rGH, but not rPRL, infusion. In intact animals of both sexes, rGH infusion significantly lowered SM-C levels by 30-40%; thus both bGH and oPRL binding in individual pituitary-intact rats were negatively correlated with serum SM-C. In rGH-treated hypophysectomized rats, induced GH (but not PRL) binding sites showed significant positive correlation with SM-C levels. The induction of GH and PRL receptors by rGH occurs independently of SM-C generation, but newly induced GH receptors in GH-treated hypophysectomized rats may be involved in SM-C generation.