Abstract
Summary and Conclusions
The effect of glucagon and of epinephrine on liver and muscle glycogen of adrenalectomized and hypophysectomized rats with or without treatment with cortisone or insulin was studied. 1) Epinephrine caused an immediate decrease in muscle glycogen in all cases and a decrease in liver glycogen in animals treated with cortisone. 2) In untreated adrenalectomized rats, liver glycogen was very low and further decrease due to epinephrine was not significant. Xo secondary increase in liver glycogen was noted. 3) Two hours after injection of glucagon, no significant changes in liver and muscle glycogen of untreated adrenalectomized or hypophysectomized animals were noted. 4) Twenty-four hours after the injection of glucagon in untreated adrenalectomized rats there was a significant, but very small increase in liver glycogen. Muscle glycogen was unchanged. No significant changes were noted in liver and muscle glycogen of untreated hypophysectomized rats. 5) In cortisone treated adrenalectomized or hypophysectomized rats, glucagon caused a significant decrease in liver glycogen, 2 hours after injection. 6) No secondary increase in liver glycogen was noted in cortisone treated hypophysectomized rats. 7) Glucagon caused a secondary increase in liver glycogen in cortisone treated adrenalectomized rats and in hypophysectomized rats treated with insulin. 8) No significant changes in muscle glycogen of treated or untreated rats were noted following glucagon injection. 9) The results are consistent with the hypothesis that glycogenolysis and hyperglycemia are the primary effects of glucagon and epinephrine and that the delayed increase in liver glycogen and occasionally of muscle glycogen, observed after injection of these hormones, is the result of a secondary secretion of insulin aided by the “permissive” action of the adrenal cortex. 10) The importance of time factors in this “rebound” phenomenon is emphasized.
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