Abstract
THE hyperglycemia and glycosuria produced by epinephrine described half a century ago as “adrenalin diabetes”—has been generally attributed to an increase in the rate of hepatic glycogenolysis. This concept is based on considerable, and apparently unequivocal, experimental evidence. It is well known, for instance, that in hepatectomized animals epinephrine does not produce hyperglycemia, and that in the perfused liver and in liver slices in vitro glucose output in increased by epinephrine. In a recent paper (Somogyi, 1950) we called attention to another, well defined phase of epinephrine action, namely inhibition of glucose assimilation,1 as a factor that contributes to epinephrine hyperglycemia. In that paper we confirmed the earlier findings of Wilenko (1913), Wiechman (1927), and Cori et al. (1928 and 1935), to the effect that epinephrine greatly depresses the rate of peripheral glucose assimilation. We expressed the view that this is a factor which potently enhances hyperglycemia.
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