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. 1976;3(3-4):199-208.
doi: 10.3109/07435807609056900.

Induction of lactogenic receptors. II. Studies on the liver of hypophysectomized male rats and on rats bearing a growth hormone secreting tumor

C Aragona, H G Bohnet, V S Fang, H G Friesen

Induction of lactogenic receptors. II. Studies on the liver of hypophysectomized male rats and on rats bearing a growth hormone secreting tumor

C Aragona et al. Endocr Res Commun. 1976.

Abstract

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.

PIP: The role of growth hormone (GH), prolactin (PRL), and adrenocorticotropic hormone (ACTH) in the induction of the PRL receptor was investigated in hypophysectomized male rat livers and in the livers of male rats bearing a GH secreting tumor. After 7 days of sc injections, specific binding of PRL in controls and rats treated with PRL, GH, ACTH, human chorionic gonadotropin, estradiol, or testosterone was approximately 1%. Treatment with PRL plus ACTH increased specific binding to 4%; adding estradiol to this combination produced a further increase to 8%, whereas the addition of testosterone decreased hepatic binding to 1%. Combination of GH with ACTH was most effective giving a specific binding of 33%, which is similar to the 36% observed in the liver of rats bearing a GH-secreting tumor. These results 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.

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