Cardiac membrane lipid composition and adenylate cyclase activity following dietary eicosapentaenoic acid supplementation in the marmoset monkey

Abstract

The effects of dietary eicosapentaenoic acid (20:5(n-3)) on cardiac membrane phospholipid fatty acid composition and membrane-associated adenylate cyclase activity were investigated in the marmoset monkey. A 20:5(n-3) concentrate (as the ethyl ester) was tested with high fat diets formulated to give a polyunsaturated:monounsaturated:saturated (P:M:S) fatty acid ratio of either 1:1:1 (control diet, no added cholesterol) or 0.1:0.6:1.0 (atherogenic-type diet, 0.2% cholesterol) that were fed for 30 weeks. The various dietary lipid treatments did not alter the proportions of the major phospholipids present in cardiac membranes. Both 20:5(n-3)-supplemented diets resulted in an increase in the proportions of 20:5(n-3) and 22:5(n-3), but not 22:6(n-3) in membrane phospholipids and a decrease in the proportion of 18:2(n-6) and 20:4(n-6). Greater incorporation of the n-3 polyunsaturated fatty acids occurred when the level of dietary linoleic acid was reduced. These changes in fatty acid profiles were evident to a greater extent in phosphatidylcholine and phosphatidylethanolamine in comparison with cardiolipin and sphingomyelin. These diets did not influence catecholamine-stimulated adenylate cyclase activity in terms of sensitivity or responsiveness to isoproterenol. The response of adenylate cyclase to other agonists such as epinephrine, norepinephrine, sodium fluoride, and forskolin was also unaffected by the dietary lipid treatments. The results clearly show that there is extensive incorporation of dietary 20:5(n-3) and its elongation product 22:5(n-3) into cardiac membrane phosphatidylcholine and phosphatidylethanolamine. However, unlike the reported effect of altered cardiac membrane cholesterol status, alterations in cardiac membrane phospholipid fatty acid composition alone appear not to affect membrane-associated adenylate cyclase activity in the marmoset monkey.