Effect of Dietary Ethanol and Cholesterol on Phospholipid Composition of Hepatic Mitochondria and Microsomes from the Monkey, Macaca nemestrina

Monkeys (Macaca nemestrina) were divided into four groups, and each group was fed a particular diet. The variables in the diets were as follows: diet A, 0.3 mg cholesterol/kcal nutrient; diet B, 1.0 mg cholesterol/kcal nutrient; diet C, 0.3 mg cholesterol/kcal nutrient, ethanol (36% of calories); diet D, 1.0 mg cholesterol/ kcal nutrient, ethanol (36% of calories). Monkeys on the diets containing ethanol developed fatty liver. Mitochondria and microsomes isolated from these livers demonstrated ethanol-elicited alterations in metabolic functions as is described in the preceding paper.¹ Accompanying these changes in metabolic activities were alterations in organelle phospholipids that were influenced by both dietary ethanol and cholesterol. The changes that could be attributed to ethanol were as follows. Phosphatidyl ethanolamine was decreased in microsomes and increased in mitochondria; the sphingomyelin content in microsomes was increased significantly. The levels of stearic and arachidonic acid were elevated, and palmitic and oleic acid decreased, in phospholipids from both mitochondria and microsomes. Cholesterol influenced the fatty acid composition of several phospholipids, usually in a direction opposite to those alterations attributed to ethanol. Cholesterol feeding increased levels of palmitic and oleic acid and decreased amounts of stearic, linoleic, and arachidonic acid in several phospholipids. The significant ethanol- and cholesterol-elicited alterations observed in this study suggest the possibility that the changes in metabolic functions in mitochondria and microsomes are controlled, at least in part, by alterations in the phospholipid compositions of these organmicrosomes are controlled, at least In part, by alterations in the phospholipid compositions of these organelles.