Effects of 17β-estradiol and starvation on trout plasma lipoproteins

Administering 17β-estradiol (E2) to juvenile trout results in plasma hyperlipidemia and hyperlipoproteinemia associated with significant increases in the concentrations of triglycerides (TG), free cholesterol, phospholipids, free fatty acids and proteins, both postprandial and during starvation. TG undergo the greatest increase (9 times control level 96 h after feeding). The concentration differences between E2-treated and control trout increase during starvation, primarily by progressive decreases in the concentrations of various lipids in controls. E2-induced hypertriglyceridemia is mainly caused by an increase in the concentration of very low density lipoproteins (VLDL) during both the postprandial period (6 times control level at 24 h) and during starvation (15 times control level at 96 h); hyperlipoproteinemia lasts up to at least 7 d after the last feeding. E2 treatment does not change the concentration of high density lipoproteins, but does increase plasma concentrations of a very high density lipoprotein, vitellogenin (VTG). In E2-treated VLDL, cholesteryl esters are depleted while proteins are enriched. During the postprandial phase, the apolipoprotein (apo) profile of VLDL (d< 1.015 g/mL) is comparable in E2-treated and control trout. Starvation of E2-treated trout is accompanied by an enrichment in apo B240, A-I and A-II. The secretion levels of TG and VLDL-TG, as determinedin vivo, by injecting Triton WR-1339 to starving animals, are significantly higher in E2-treated trout than in controls. In trout, as in chicks, E2 administration significantly increases the concentration and hepatic secretion of plasma VLDL independent of the nutritional status and the appearance of VTG in the plasma. This suggests the existence of similar mechanisms for the regulation of lipoprotein metabolism by estrogens in oviparous vertebrates.