AJP - Endocrinology and Metabolism, Vol 262, Issue 4 E434-E439, Copyright © 1992 by American Physiological Society
Effect of hypercorticism on regulation of skeletal muscle glycogen metabolism by epinephrine
L. Coderre, A. K. Srivastava and J. L. Chiasson
Clinical Research Institutes of Montreal, University of Montreal, Quebec, Canada.
The effect of hypercorticism on the regulation of glycogen metabolism by
epinephrine was examined in skeletal muscles using a hindlimb perfusion
technique. Rats were injected with either saline or dexamethasone (0.4
mg.kg-1.day-1) for 14 days and were studied in the fed and fasted (24 h)
states under saline or epinephrine (10(-7) M) treatment. In the fed state,
dexamethasone administration did not affect basal glycogen concentration
but decreased glycogen synthase activity ratio in white and red
gastrocnemius muscles. Epinephrine failed to decrease glycogen content
despite the expected activation of glycogen phosphorylase in the fed
dexamethasone-treated rats. Dexamethasone treatment resulted in a threefold
increase in the level of muscle adenosine, a phosphorylase a inhibitor. In
control rats, fasting was associated with a decrease in muscle glycogen
concentration (P less than 0.01) and with an increase in the glycogen
synthase activity ratio. Dexamethasone treatment, however, totally
abolished both the decreased muscle glycogen content and glycogen synthase
activation observed in fasting controls. In the dexamethasone-treated
group, fasting restored the glycogenolytic effect of epinephrine.
Interestingly, it was associated with decreased muscle adenosine
concentrations. These data indicate that, in the fed state, dexamethasone
treatment inhibits skeletal muscle glycogenolysis in response to
epinephrine despite phosphorylase activation and glycogen synthase
inactivation. It is suggested that this abnormality could be due to the
inhibition of phosphorylase a by increased muscle adenosine levels.
