Lipoprotein alterations in the spontaneously hypertensive rat fed diets deficient in selenium and vitamin E.

Both vitamin E and selenium (Se) are antioxidant nutrients that play important roles in preventing in vivo lipid peroxidation. In this investigation, Se and vitamin E were found to influence lipoprotein levels in the spontaneously hypertensive rat (SHR). Four-week-old inbred SHRs were fed a basal (B) diet with 1% cholesterol deficient in both selenium and vitamin E (B+cho diet) or identical diets to which either vitamin E (B+E+cho) or selenium (B+Se+cho) or both micronutrients were added (B+Se+E+cho). Plasma-cho and lipoprotein-cho levels were measured after 6, 12, 16, and 18 weeks of feeding the experimental diets. Rats fed the B+cho diet for at least 12 weeks had plasma-cho levels about twice that observed for rats fed the B+E+Se+cho diet. Plasma-cho levels for rats in the two Se deficient groups (B+cho and B+E+cho) were, however, similar at any time point. Se deficiency was associated with increased plasma-cho, very low density lipoprotein-cho (VLDL-cho) and low-density lipoprotein-cho (LDL-cho). Vitamin E supplementation interacted with Se deficiency to increase plasma VLDL-cho levels. Neither vitamin E alone nor the interaction between vitamin E and Se consistently influenced LDL-cho levels. The percent cholesteryl ester in LDL from rats fed the Se-deficient diets (B+cho or B+E+cho) was at least twice that observed for rats fed the B+E+Se+cho diet. Plasma lipid peroxidation products were highly elevated in rats fed the B+cho diet compared with values for the B+E+cho or the B+E+Se+cho fed rats (which were not significantly different). These results suggest that dietary Se deficiency increases plasma-cho, VLDL-cho, and LDL-cho levels by a mechanism that may be unrelated to its role as an antioxidant nutrient.

The role of selenium in the secretion of very-low-density lipoprotein in the isolated perfused rat liver.

A recirculating liver perfusion system was used to study the effects of dietary selenium (Se) on the hepatic secretion of very-low-density lipoprotein (VLDL). The perfusate from livers of rats fed on a Se-deficient diet incorporated about 50% more [1-14C]oleic acid into triacylglycerol (TG) and cholesteryl esters (ChoEs) than did the perfusate from livers of rats fed on a Se-supplemented diet. Similarly, livers from rats fed the Se-deficient diet secreted more VLDL and incorporated about 60% more [1-14C]oleic acid into VLDL TG and ChoEs than did livers from rats fed the Se-supplemented diet. The liver perfusate from rats in the Se-deficient group also showed significantly decreased fatty acid oxidation. We conclude that Se is a potent modulator of lipoprotein metabolism. A primary action of Se deficiency appears to be a decrease in fatty acid oxidation and a stimulation of fatty acid esterification, leading to increased VLDL TG and ChoEs formation and secretion.