Abstract
ALTHOUGH it is generally believed that the hyperglycæmia which follows the administration of epinephrine is due, at least in part, to hepatic glycogenolysis, attempts to demonstrate a direct effect of epinephrine on liver glycogen-levels have led to conflicting conclusions. In the rat, for example, Cori, Cori and Buchwald1 found that a decrease in liver glycogen occurred during the first 15 min after subcutaneous epinephrine injection, and considered this to represent a direct action of epinephrine on the liver. On the other hand, Sherlock2 found that portal veining infusions of epinephrine did not affect liver glycogen- or blood glucose-levels and concluded that the hormone did not exert a direct effect on hepatic glycogen metabolism of rats. We repeated and extended the experiments of Cori, Cori and Buchwald and also observed the transient hepatic glycogenolysis which they had described3. However, we presented evidence that this represented an indirect rather than a direct effect of epinephrine and suggested that it might be due to stimulation of endogenous glucagon release.
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References
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SOKAL, J., SARCIONE, E. Failure of Physiological Concentrations of Epinephrine to affect Glycogen-levels in the Isolated Rat Liver. Nature 204, 881–883 (1964). https://doi.org/10.1038/204881a0
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DOI: https://doi.org/10.1038/204881a0
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