Abstract
Insulin and epinephrin are frequently considered as antagonistic because hypoglykemia and hyperglykemia follow after the respective administration of these substances.
Since we know the mechanism of insulin action, 1 the alleged antagonism of insulin and epinephrin gained interest for us. We have previously demonstrated that insulin has a two-fold action depending upon whether or not insulin is absorbed at the site of injection. 2
From a tissue depôt (an intradermal injection) insulin acts purely by nerve stimulation, increasing the glycogenetic function of the liver. This glycogenesis finds its expression in a consequent lowering of the blood sugar. Insulin absorbed from its tissue depôt, or injected intravenously does not bring about this glycogenetic action.
Insulin injected intravenously or absorbed from a subcutaneous injection becomes effective after making contact with the tissues of the body. This process is one that takes a certain period of time, and the effect will not be noted for 30 to 40 minutes after injection, while the nerve action is immediate. Insulin injected subcutaneously or intravenously, for comparison with epinephrin action, will enable us to compare only the hormone action of insulin, i. e., its glycolytic action, with the effect of epinephrin. Such an antagonism is quite improbable. The antagonistic process would consist of building up sugar.
Pertinent experiments of MacLeod and his associates 3 have been made as follows: Epinephrin was given to animals one hour after insulin injection, with a resulting equalization of both insulin and adrenalin effect on the blood sugar. We do not believe that this observation justifies the assumption of an antagonistic effect of epinephrin and insulin.
In a series of animals we have first determined the relative dosage of epinephrin and insulin which would produce a corresponding percentage augmentation or reduction, respectively, of blood sugar.
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