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Effect of Dietary Fat on the Utilization of Fatty Acids by Myocardial Tissue in the Rat¹

Nutrition and Metabolism Research Group, Department of Foods and Nutrition, University of Alberta, Edmonton, T6G 2M8 and Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada M5S 1A8

Weanling rats were fed high fat diets containing 40% of energy as fat for 23 d. Diets were formulated to contain equivalent content of essential nutrients per calorie for the nonfat components. Four oil mixtures provided high dietary levels of either oleic, linoleic, linolenic or erucic acid. Effect of dietary fatty acid composition on the fatty acid composition of phosphatidylcholine, phosphatidylethanolamine and cardiolipin isolated from cardiac mitochondria was examined in conjunction with the effect of diet on the oxidative activity of cardiac mitochondria. Dietary treatments that reduced the content of C16:0 in the sn-1 and sn-2 positions of phosphatidylcholine were associated with increased content of C20:1 and C22:1 fatty acids into the sn-2 position and resulted in decreased oxidative activity of cardiac mitochondria utilizing palmitylcarnitine as a substrate for oxidation. Diets high in linoleic acid did not increase membrane phospholipid content of 3 fatty acids, but resulted in decreased level of C20:46. In a subsequent perfusion experiment, hearts were removed from animals fed either high erucic or high linoleic acid diets and were perfused to examine rates of fatty acid oxidation and simultaneous synthesis of high energy phosphate compounds in cardiac muscle. Diet did not affect the levels of creatine phosphate or adenine nucleotides present in the tissue on a per-gram-wet-weight basis, but production of ¹⁴CO₂ from ß-oxidation of palmitic acid was lower for animals fed the high erucic acid diet than for those fed the high linoleic acid diet. Since this diet did not alter oxidation of palmitylcarnitine in vitro and as ß-oxidation of lauric acid was not decreased in the perfused heart, we conclude that mitochondrial oxidation of fatty acid was not altered by diet and that low rates observed for palmitate oxidation are attributable to reduced palmitylcarnitine synthesis.

KEY WORDS: • rats • fatty acid • phospholipid • mitochondrial oxidation • ß-oxidation • perfusion • heart

¹ The research was financially supported by the Natural Sciences and Engineering Research Council of Canada, the Farming for the Future program through Alberta Agriculture, and the Ontario Heart Foundation.

² Sung-Hee Cho Lee's address is: Department of Food Science and Nutrition, Hyosung University, 1155 Bongduk-Dong, Nam-Gu, Taegu, Korea.

³ Reprint requests should be made to Dr. M. T. Clandinin at the first address. Dr. Clandinin is presently a Scholar of the Alberta Heritage Foundation for Medical Research.

Manuscript received 28 May 1985. Revision accepted 9 June 1986.