Concurrent inductions of avian hepatic lipogenesis, plasma lipids, and plasma apolipoprotein B by estrogen.

The inductions of hepatic fatty acid synthesis, estrogen-specific plasma proteins, plasma lipids, and apolipoproteins by a single subcutaneous injection of diethylstilbestrol (40 mg/kg body weight) have been examined in immature male turkeys. Estrogen induced the appearance of phosvitin, lipovitellin, and apoVLDL-II in the blood plasma. The highest concentrations of these estrogen-specific plasma proteins were observed 48 hr following hormone administration. Estrogen increased the concentration of triglyceride in the liver, predominantly those molecular species containing 16 carbon fatty acids (triglycerides with 53 and 55 carbon atoms). Liver cholesterol was present predominantly as free cholesterol. Although estrogen did not affect the concentrations of free or esterified cholesterol in the liver, the hormone increased the amount of cholesterol esterified with 20-carbon fatty acids and caused a corresponding decrease in cholesterol esterified with 18 carbon fatty acids. Estrogen treatment elevated the plasma triglycerides 55-fold, tripled the plasma phospholipid, and approximately doubled the plasma cholesterol. The de novo synthesis of fatty acids in the liver in vivo was stimulated by estrogen administration, as exhibited by increased 3H2O incorporation into the phospholipids and triglycerides of both liver and plasma. In contrast, hepatic cholesterol synthesis was unaffected. The amounts of newly synthesized triglyceride in the liver and plasma and the specific radioactivities of the plasma triglyceride following 1-hr in vivo labeling periods, 0, 24, 48, and 72 hr after estrogen injection indicate that increased hepatic fatty acid synthesis is a primary and major casuative factor in the development of estrogen-induced hyperglyceridemia in this avian species. The concentration of apolipoprotein B in the plasma increased in parallel with hepatic fatty acid synthesis and the appearance of newly synthesized triglyceride in the plasma, whereas the plasma apolipoprotein A-I level decreased. These observations indicate that in the avian liver estrogen causes a coordination of inductions in the conversion of carbohydrate to triglyceride and in the production of proteins (apolipoprotein B and apoVLDL-II) involved in the assembly of triglyceride-rich lipoprotein particles, leading to hypersecretion of these lipoproteins into the circulation.