Dietary ethanol-induced modifications in hyperlipoproteinemia and atherosclerosis in nonhuman primates (Macaca nemestrina).

Male Macaca nemestrina were studied in an experiment with a 2 x 2 factorial design. Diets contained low vs high cholesterol levels (0.3 vs 1.0 mg/Kcal) and no ethanol or ethanol, as 36% of the calories substituted isocalorically for carbohydrate. After receiving their diets for 18 months, the monkeys had blood samples drawn for lipoprotein analyses, and then were killed for evaluation of the extent of atherosclerosis. Ethanol-fed groups had significantly increased concentrations of serum cholesterol, triglycerides, low density lipoprotein, and high density lipoprotein. The molecular weight of the low density lipoprotein particles was lower in ethanol-fed animals and the cholesterol esters of low density lipoprotein and high density lipoprotein contained relatively more cholesteryl linoleate and less cholesteryl oleate. Dietary cholesterol had the effect of increasing the concentration of low density lipoprotein (primarily via increasing the low density lipoprotein molecular weight) and decreasing the concentration of high density lipoprotein. Significant interactions were found between the effects of ethanol and cholesterol on high density lipoprotein and low density lipoprotein. Ethanol significantly decreased the cholesterol-induced atherosclerosis found in the aorta and coronary arteries. Highly significant correlations between coronary artery atherosclerosis and low density lipoprotein cholesterol ester pattern were found. In contrast, low density lipoprotein molar concentration (number of low density lipoprotein particles per liter of plasma) was not significantly correlated with coronary artery atherosclerosis. Different relationships with aortic atherosclerosis were found; low density lipoprotein molecular weight and cholesterol ester pattern were highly correlated, while high density lipoprotein concentration was not. The high correlations found between lipoprotein characteristics and atherosclerosis severity have been mediated through its effects on the plasma lipoproteins.