Abstract
Previous experiments1 have led to the conclusion that one of the principal causes for the epinephrine hyperglycemia consists in a decreased utilization of blood sugar in the tissues. It was pointed out that mobilization of liver glycogen alone is an inadequate explanation for the hyperglycemia, because there is not enough liver glycogen present to provide the tissues for hours with sugar at a rate which is greater than their normal ability to utilize sugar. Mobilization of liver glycogen can only lead to a protracted hyperglycemia of the type observed after epinephrine injections, (1) if a new formation of liver glycogen occurs which keeps pace with the conversion of liver glycogen into blood sugar and (2) if utilization of blood sugar itself is diminished. A new formation of liver glycogen exceeding its mobilization was demonstrated during epinephrine action and the source for the newly formed liver glycogen was found to be lactic acid derived from muscle glycogen.1 That blood sugar utilization is low du...
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