A comparison between the effects of growth hormone on prolactin receptors and estrogen receptors in rat liver.

Abstract

Human GH (hGH) increased hepatic PRL and estrogen receptors in hypophysectomized (Hx) female rats after continuous infusion of the hormone (5 micrograms/h) using osmotic minipumps, but not after the infrequent administration of the same daily dose (120 micrograms) of the hormone by sc injections (60 micrograms/12 h). The effects of hGH on body weight (an increase) and tibial epiphyseal zones (a widening) were observed regardless of the mode of hGH administration. Thus, it would seem as if the mode of administration of hGH is of importance for the type of biological effect exerted by the hormone. Furthermore, rGH was effective in increasing both PRL and estrogen receptors in the liver of Hx ovariectomized (HxOx) rats, whereas rat PRL (rPRL) was much less efficient. Finally, rat GH (rGH) suppressed the concentration of a nonreceptor estrogen-binding protein in the liver of HxOx rats; the protein occurred at a low concentration in Ox rats and was markedly increased after hypophysectomy rPRL was inefficient in modulating the concentration of estrogen-binding protein. Thus, rGH, but not rPRL, seems to regulate both sexually differentiated (PRL receptors and estrogen-binding protein) and sexually nondifferentiated (estrogen receptor) functions in the rat liver. The mechanism behind this dual effect of rGH is obscure, but may possibly be related to the presence of isohormones of rGH with different effects on the liver.