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AJP - Endocrinology and Metabolism, Vol 255, Issue 1 E1-E8, Copyright © 1988 by American Physiological Society
ARTICLES |
P. F. Mohan and M. P. Cleary
Hormel Institute, University of Minnesota, Austin 55912.
Lean and obese Zucker rats, 7-8 wk of age, were treated with dehydroepiandrosterone (DHEA) for either 3 or 7 days to determine the initial cellular event(s) that might be responsible for the antiobesity activity of DHEA. Epididymal, retroperitoneal, and brown adipose tissue weights were unaltered by either 3 or 7 days of DHEA treatment. Liver weight was not affected by 3 days of treatment but was 13 and 18% higher in 7-day DHEA-treated lean and obese rats, respectively, compared with their corresponding control group. Mitochondrial state 3 respiration rates with glutamate-malate and succinate as substrates were elevated by an average of 35% in 3- and 7-day DHEA-treated obese rats and by 15-20% in 7-day DHEA-treated lean rats compared with rates obtained in the corresponding control groups. State 3 respiration was not affected in 3-day DHEA-treated lean rats compared with control lean rats. The specific activities of long-chain fatty acyl-coenzyme A synthase and hydrolase and the levels of free CoA were increased by severalfold in cellular fractions of both DHEA-treated lean and obese rats compared with their respective control group. Hepatic malic enzyme activity, which was shown earlier to be elevated with long-term DHEA treatment, was unaltered by either 3 or 7 days of DHEA administration. The above results suggest the involvement of mitochondrial respiration and fatty acid deacylation/reacylation in the antiobesity mechanism of action of DHEA.
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P. A. Hansen, D. H. Han, L. A. Nolte, M. Chen, and J. O. Holloszy DHEA protects against visceral obesity and muscle insulin resistance in rats fed a high-fat diet Am J Physiol Regulatory Integrative Comp Physiol, November 1, 1997; 273(5): R1704 - R1708. [Abstract] [Full Text] [PDF] |
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