[Studies on ontogenesis and the regulatory mechanism of hPL binding factor (hPL receptor) in rat liver (author's transl)].

Abstract

Ontogenesis of hPL binding factor and its regulatory mechanism were investigated in rat liver cell membranes. The results were as follows: 1) Binding of hPL was very low in liver cell membranes from fetal and immature rats. It began to increase after 28 days of age. It increased over control level at mid-pregnancy (L12), reaching more than 300--400% of control level in late pregnancy. It decreased immediately to control level within 24hrs. after parturition. 2) Among the rats treated with estradiol-17 beta, those with progesterone, or those with hydrocortisone, the binding showed a dose-dependent increase in the rats treated with estradiol but no significant change in the others. Combined administration of estradiol and dexamethasone suppressed the binding increased by estradiol completely. 3) The binding was not be able to detected 7 days after hypophysectomy in rats. hPL treatment with PVP (polyvinylpyrrolidone) could restore them. On the other hand, estradiol-17 beta treatment failed to restore. 4) Estradiol-17 beta, progesterone, corticosterone, rPRL, and rCM (rat chorionic mammotropin) were measured in rats in pregnancy. The level of rCM elevated with two peaks at mid-pregnancy and at near term. The other hormones were not changed. In conclusion, hPL binding factor (hPL receptor) in rat liver cell membrane have an intimate relation with maturity and pregnancy. The receptor or its function may be induced by hPL itself and estrogen, but suppressed by glucocorticoid.