AJP - Endocrinology and Metabolism, Vol 262, Issue 4 E427-E433, Copyright © 1992 by American Physiological Society
Effect of hypercorticism on regulation of skeletal muscle glycogen metabolism by insulin
L. Coderre, A. K. Srivastava and J. L. Chiasson
Clinical Research Institute of Montreal, University of Montreal, Quebec, Canada.
The effects of hypercorticism on the regulation of glycogen metabolism by
insulin in skeletal muscles was examined by using the hindlimb perfusion
technique. Rats were injected daily with either saline or dexamethasone
(0.4 mg.kg-1.day-1) for 14 days and were studied in the fed or fasted (24
h) state under saline or insulin (1 mU/ml) treatment. In fed controls,
insulin resulted in glycogen synthase activation and in enhanced glycogen
synthesis. In dexamethasone-treated animals, basal muscle glycogen
concentration remained normal, but glycogen synthase activity ratio was
decreased in white and red gastrocnemius and plantaris muscles.
Furthermore, insulin failed to activate glycogen synthase and glycogen
synthesis. In the controls, fasting was associated with decreased glycogen
concentrations and with increased glycogen synthase activity ratio in all
four groups of muscles (P less than 0.01). Dexamethasone treatment,
however, completely abolished the decrease in muscle glycogen content as
well as the augmented glycogen synthase activity ratio associated with
fasting. Insulin infusion stimulated glycogen synthesis in fasted controls
but not in dexamethasone-treated rats. These data therefore indicate that
dexamethasone treatment inhibits the stimulatory effect of insulin on
glycogen synthase activity and on glycogen synthesis. Furthermore,
hypercorticism suppresses the decrease in muscle glycogen content
associated with fasting.
