Suppressive effect of glucose administration on the binding of prolactin by rat liver

Abstract

In an attempt to elucidate the physiologic role of the hepatic receptors for prolactin (PRL), we studied the effect of changes in diet on the specific binding of 125I-ovine prolactin (oPRL) by membranes from female rat liver. Specific binding of PRL (SBP) was decreased by over 50% in rats fed 15% glucose ad lib for 2 days, as compared with fasted rats ( P < .01), while serum PRL was similar in both groups. Feeding 20% glucose by tube decreased SBP significantly, but tube-feeding equicaloric amounts of rat or protein-amino acid solution did not. Glucose feeding did not decrease the specific binding of 125I-bovine growth hormone (bGH) to liver, or decrease SBP to membranes of nitrosomethylurea (NMU)-induced mammary carcinomas, indicating that the effect of glucose on hepatic SBP is selective. Administration of glucose decreased SBP significantly in adrenalectomized-ovariectomized rats, in adrenalectomized-chemically sympathectomized rats, and in hypophysectomized rats receiving replacement therapy, including bovine prolactin (bPRL), bGH, hydrocortisone, estrogen, and thyroid hormones. Thus, the effect of glucose is not mediated by a factor from the adrenals, ovaries, or pituitary, and probably not by catecholamines. Administration of insulin to fasted diabetic rats did not alter SBP. Infusion of glucagon for 1 day, at a rate that did not alter serum glucose, increased hepatic SBP 29% ( P < .01). Since glucose administration decreases plasma glucagon, we hypothesize that glucagon may contribute to the maintenance of the hepatic PRL receptors, and that the suppressive effect of glucose on hepatic SBP may be mediated at least in part by suppression of plasma glucagon. The present observations raise the possibility that in the female rat, the hepatic PRL receptors are involved in the metabolic response of the liver to alterations in carbohydrate intake.