Induction of lactogenic receptors. II. Studies on the liver of hypophysectomized male rats and on rats bearing a growth hormone secreting tumor.
The role of growth hormone (GH), as well as prolactin and ACTH, in the induction of the PRL receptor was investigated both in hypophysectomized male rat livers and in the livers of male rats bearing a GH secreting tumor. After 7 days of s.c. injections, specific binding (% SB) of PRL in controls and rats treated with oPRL, hGH, ACTH, hCG, estradiol (E2), or testosterone (T) was approximately 1%. Treatment with oPRL plus ACTH increased SB to 4%; adding E2 to this combination produced a further increase to 8%, whereas the addition of T decreased hepatic binding to 1%. Combination of hGH with ACTH was most effective, giving a SB of 33%, which is similar to that observed in the liver of rats bearing a GH secreting tumor (36%). These studies suggest that GH acts synergistically with PRL and/or ACTH to increase lactogenic binding sites in the male rat liver and that sex steroids have a modulating effect on this action.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D004958:Estradiol / Q000494:pharmacology; D013006:Growth Hormone / Q000378:metabolism* / Q000494:pharmacology; D007016:Hypophysectomy; D008099:Liver / Q000378:metabolism*; D008297:Male; D010911:Pituitary Neoplasms / Q000378:metabolism*; D011388:Prolactin / Q000378:metabolism* / Q000494:pharmacology; D051381:Rats; D011956:Receptors, Cell Surface / Q000096:biosynthesis*; D013739:Testosterone / Q000494:pharmacology
D011956:Receptors, Cell Surface; D013739:Testosterone; D004958:Estradiol; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D013006:Growth Hormone