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Effect of High Fat Diets on Energy Balance and Thermogenesis in Brown Adipose Tissue of Lean and Genetically Obese ob/ob Mice

Dunn Nutrition Laboratory, Medical Research Council and University of Cambridge, Cambridge CB4 1XJ, United Kingdom

The effects on energy balance and brown adipose tissue thermogenesis of feeding high fat diets of differing fatty acid composition have been investigated in lean and genetically obese (ob/ob) mice. Groups of mice were fed either a low fat diet or a high fat diet based on corn oil or beef tallow for 2 wk. Energy intake and body weight gain were higher in both lean and obese animals fed the high fat diets than in respective mice fed the low fat diets. Carcass energy gain was greater for the obese than for the lean consuming each of the diets. Both lean and obese mice had a higher energy gain when fed the beef tallow diet than when fed the corn oil, despite isoenergetic intakes of the two diets. The thermogenic activity of brown adipose tissue, assessed from measurements of cytochrome oxidase activity and mitochondrial guanosine 5'-diphosphate (GDP) binding, were greater in both lean and obese mice fed the corn oil diet than in those fed the low fat diet. However, GDP binding and cytochrome oxidase activities in lean or obese mice fed the beef tallow diet were not different from those of mice of the same genotype fed the low fat diet. These results indicate that in both lean and obese (ob/ob) mice energy deposition and the stimulation of brown adipose tissue thermogenesis during the voluntary hyperphagia induced by feeding high fat diets are influenced by the fatty acid composition of the diet. A diet rich in polyunsaturated fatty acids appears to result in preferential stimulation of the thermogenic activity of brown adipose tissue, particularly in the ob/ob mouse.

KEY WORDS: • brown adipose tissue • diet-induced thermogenesis • obese mouse • dietary fat • polyunsaturated fatty acids

¹ S.W.M. received a Research Studentship funded by Unilever PLC.

² Present address: Metabolic Research Laboratory, Nuffield Department of Clinical Medicine, Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE, U.K.

³ To whom correspondence should be directed at the present address: Nutrition and Metabolism Research Group, 536 Newton Research Building, University of Alberta, Edmonton, Alberta, Canada T6G 2C2.

Manuscript received 18 June 1987. Revision accepted 31 August 1987.

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