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The Effect of Dehydroepiandrosterone on Liver Metabolites

National Institute on Alcohol Abuse and Alcoholism, 12501 Washington Avenue, Rockville, MD 20852

Liver metabolites and in vitro enzyme activities were measured in Sprague-Dawley rats pair-fed the standard NIH diet with or without 0.6% (wt/wt) dehydroepiandrosterone (DHEA) for 16 d. Absorption of DHEA from the gut was confirmed by a 300-fold increase in urine 17-ketosteroids in DHEA-treated animals. Of the liver metabolites measured only 6-phosphogluconate was significantly changed, increasing by less than a factor of two in the DHEA-treated animals, 38.7 ± 2.2 nmol/g, above the value in the pair-fed controls, 22.5 ± 2.5 nmol/g. Contrary to the in vitro findings that DHEA inhibits glucose-6-phosphate dehydrogenase (EC 1.1.1.49), thus leading to the hypothesis that DHEA inhibits fat synthesis by diminishing the availability of NADPH, the [NADP⁺]/[NADPH] ratios calculated from the 6-phosphogluconate dehydrogenase (EC 1.1.1.44), isocitrate dehydrogenase (EC 1.1.1.42) and malic enzyme (EC 1.1.1.40) redox couples were no more oxidized in the DHEA-treated animals than in the control animals. Malic enzyme and isocitrate dehydrogenase activities were 620 and 25% higher in DHEA-treated animals than in pair-fed controls. There was no change in the measured activity of glucose-6-phosphate dehydrogenase or 6-phosphogluconate dehydrogenase. These data give no support to the hypothesis that administration of DHEA per os results in decreased cytoplasmic NADPH in liver.

KEY WORDS: • dehydroepiandrosterone • pentose cycle • NADPH • malic enzyme

Manuscript received 14 January 1985. Revision accepted 14 October 1985.