Epinephrine enhances glycogen turnover and depresses glucose uptake in vivo in rat heart

In vivo effects of epinephrine on glucose uptake and glycogen turnover in rat heart were studied and compared to liver and skeletal muscle. Fasted ketamine-anesthetized rats were intravenously infused with saline or epinephrine. Both the low and high doses of epinephrine resulted in hyperglycemia (40-50%) and hyperlactemia (threefold) at the end of infusion. Glucose uptake, determined by the phosphorylation of the intravenously injected [¹⁴C] 2-deoxyglucose, was found to decrease in the heart and skeletal muscle of epinephrine-infused rats. Glycogen in livers, skeletal muscles, and hearts of the epinephrine-infused rats decreased to varying degrees relative to the saline-infused rats, indicating enhanced glycogenolysis in all three organs. Glycogen synthesis, determined by the incorporation of the co-infused [3-³H]glucose into glycogen, was found to decrease in liver and skeletal muscle. However, glycogen synthesis in the heart was found to increase 50% in Epi-1 and 280% in Epi-2 compared to the saline-infused rats. We conclude that glucose utilization in the in vivo heart may be preferentially channeled through glycogen turnover in the presence of epinephrine. That both synthesis and degradation of glycogen can be simultaneously activated appears to be unique to the heart and is protective against a loss of glycogen at a time of enhanced glucose utilization.