Abstract
The ontogenesis of specific binding of 125I-hPL and 125I-insulin was determined in rat liver cell membranes (105×g pellets), and the regulatory mechanisms of these binding sites were also examined.
There were striking differences in the mode of ontogenesis between binding sites of hPL and insulin in rats. HPL binding sites were very few in liver cell membranes from fetal and immature rats. They began to increase after puberty, and markedly increased in late pregnancy. On the other hand, insulin binding sites, which decreased in late pregnancy, were dominant in fetal liver and placenta. Consequently, the lipolytic and glycogenolytic activities of hPL, in maternal liver were accentuated, whereas the effects of insulin on maternal liver were suppressed. In contrast, in fetal liver and placenta only the anabolic effects of insulin seemed conspicuous.
According to the results of experiments on in vivo administration of estradiol-17β, progesterone, hydrocortisone or hPL to intact or hypox-rats, and the measurement of serum rat chorionic mammotropin (rCM), rPRL, estradiol-17β, and insulin during pregnancy in rats, the increase in hepatic hPL binding sites observed in late pregnancy might be, at least in part, due to rCM secreted from placenta, and the decrease in insulin binding sites due to the increase in serum insulin itself in rats.
These results suggested that the process of ontogenesis of hPL and insulin binding sites in rat liver cell membranes might reflect a dramatic change from an anabolic state in the fetus to a relatively catabolic state in the mother, and that hepatic binding sites of hPL and insulin might be regulated by these hormones; hPL binding sites are regulated by an induced or up regulation mechanism, whereas insulin binding sites are regulated by a down regulation mechanism.
