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Endocrinology, doi:10.1210/endo-114-1-99
Endocrinology Vol. 114, No. 1 99-107
Copyright © 1984 by the Endocrine Society.
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Effect of Dexamethasone on Adipose Tissue and Liver Pyruvate Dehydrogenase and Its Stimulation by Insulin-Generated Chemical Mediator*

NAJMA BEGUM, HELEN M. TEPPERMAN and JAY TEPPERMAN{dagger}

Department of Pharmacology, State University of New York, Upstate Medical Center Syracuse, New York 13210

Abstract

Rats were treated with dexamethasone (50 µg/day, sc) for 4 days. Total pyruvate dehydrogenase (PDH) and insulin-stimulated PDHa activities were decreased in fat pads from dexamethasone-treated rats compared to control values. Coincubation experiments with adipocyte mitochondria, plasma membrane, and insulin demonstrated decreased stimulation of PDH in preparations from dexamethasone-treated rats. The responsiveness of the mitochondrial PDH system to insulin and control rat plasma membranes was not different in glucocorticoid-treated adipocyte preparations compared to controls. Liver mitochondria from dexamethasone-treated rats demonstrated decreased basal enzyme activity and a decreased percentage of stimulation of PDH when supernatants from insulin-exposed liver particulate fractions were tested. These experiments suggest that insulin resistance produced by glucocorticoid treatment, like that resulting from fat feeding, is accompanied by a decrease in the capacity of adipocyte and liver plasma membranes to generate PDH activator in response to insulin. (Endocrinology 114: 99, 1984)

Footnotes

* This work was supported by NIH Grant AM-05410 and USPHS Grant RR-05402.

{dagger} To whom requests for reprints should be addressed.

Received November 15, 1983.






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Copyright © 1984 by The Endocrine Society