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The Effect of Dehydroepiandrosterone Acetate on Liver Peroxisomal Enzyme Activities of Male and Female Rats¹

Department of Biochemistry, University of Oxford, Oxford OX1 3QU, England ^* Department of Animal and Nutritional Sciences, University of New Hampshire, Durham, NH 03824

The present study is a follow-up to the report that dehydroeplandrosterone (DHEA) acetate treatment in rats stimulated metabolic heat production and suppressed serum triglycerides, adiposity and weight gain without affecting food intake. Activities of peroxisomal fatty acyl-coenzyme (CoA) oxidase and catalase as well as mitochondrial citrate synthase were assayed in liver tissue of 24 young adult male and female Wistar rats fed a nonpurified diet containing 0.6% DHEA (6 g/kg) for 6 wk. DHEA-treated animals gained less weight but had heavier liver weights than did the controls. Hepatic activity of fatty acyl-CoA oxidase of the experimental male and female animal was 1058 and 946% higher, respectively, than that of the controls. For catalase activity, only the female groups were different (30%). Activity of citrate synthase was not affected by DHEA. These data support the hypothesis that the inhibitory effect of DHEA on energy storage as fat is mediated, at least in part, by increased ß-oxidation of fatty acids in peroxisomes. The peroxisomal ß-oxidation pathway is uncoupled from oxidative phosphorylation; electrons are transferred directly to molecular O₂ because of cycling of NAD/NADH resulting in the expenditure of chemical energy as heat.

KEY WORDS: • DHEA • peroxisomal enzymes • ß-oxidation • fatty acyl-CoA oxidase • catalase

¹ Supported in part by New Hampshire Agricultural Experiment Station Project No. H260, National Institutes of Health Grant No. AM-31549 and Scientific Contribution No. 1472 from the New Hampshire Agricultural Experiment Station.

² To whom reprint requests should be addressed.

Manuscript received 10 September 1986. Revision accepted 5 March 1987.

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