Independent behaviour of rat liver LDL receptor and HMGCoA reductase under estrogen treatment.

The main molecules of hepatic cholesterol homeostasis are HMGCoA reductase, the key enzyme of the biosynthetic pathway, and LDL receptor, responsible for the uptake of plasma lipoproteins. Estrogens are reported to cause hypolipidemia in mammalians inducing hepatic LDL receptor. The effect of such hormones on HMGCoA reductase is very ambiguous. The mechanism and the time-dependence of the effects of these hormones on HMGCoA reductase and LDL receptor in rat liver have been investigated at mRNA and protein levels, at different times after estrogen administration. Estrogens cause an early increase of LDLr, at both mRNA and protein level, and an increase of HMGCoA reductase, just at protein level, detectable only after 5 days. The independent behavior of LDLr and HMGCoA reductase under estrogen treatment suggests a not coordinate regulation by these hormones.