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Diet Effects on Membrane Phospholipid Fatty Acids and Mitochondrial Function in BHE Rats1

Orpheus E. Deaver, Jr., Rosemary C. Wander2, Robert H. McCusker, Jr.3 and Carolyn D. Berdanier4

Department of Foods and Nutrition, University of Georgia, Athens, Georgia 30602

The effects of feeding a 5% corn oil or coconut oil diet on the composition of hepatic phospholipid fatty acids and on hepatic mitochondrial function were studied. Male BHE weanling rats were fed a 65% starch diet containing 5% corn or coconut oil. Rats were decapitated, and hepatic tissue was used for phospholipid fatty acid analysis and for the preparation of mitochondria. Mitochondrial ATPase activity, {alpha}-glycerophosphate and malate-aspartate shuttle activity, and succinate- or pyruvate-supported respiration were determined. Livers from rats fed the coconut oil diet had more saturated phospholipid fatty acids than those from rats fed the corn oil diet. ATPase activity and the activity of the malate-aspartate shuttle were not affected by diet. The activity of the {alpha}-glycerophosphate shuttle was greater in rats fed the coconut oil diet than in rats fed the corn oil diet. Succinate-supported state 3 respiration was not affected by diet, whereas succinate-supported state 4 respiration was higher in mitochondria from rats fed coconut oil than in rats fed corn oil. Evidence of uncoupling of pyruvate-supported respiration from ATP synthesis was observed in mitochondria from rats fed coconut oil but not in rats fed corn oil. These observations suggest that the inherent tendency of the BHE rat toward looser coupling of respiration to ATP synthesis is potentiated by the feeding of the highly saturated fat, hydrogenated coconut oil.


KEY WORDS: • BHE rats • mitochondrial oxidation • membrane lipids • diabetes

1 Supported in part by Georgia Agricultural Experiment Station project H779 and National Institutes of Health Grant No. AM21667.

2 Present address: Department of Food Science and Nutrition, Mississippi State University, Starkville, MI 39762.

3 Present address: Clinical Research Unit, Box 501, North Carolina Memorial Hospital, Chapel Hill, NC 27514.

4 To whom correspondence should be addressed.

Manuscript received 16 August 1985. Revision accepted 24 February 1986.




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Am J Physiol Cell Physiol, September 1, 2007; 293(3): C830 - C836.
[Abstract] [Full Text] [PDF]




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