A STUDY ON THE SPECIFICITY OF THE ANTI-INSULIN EFFECT

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Abstract
IT WAS FIRST SUGGESTED by Jensen and Grattan (1) that the anti-insulin (glycotropic2) effect of the anterior pituitary may be attributed to the adrenocorticotropic principle of that gland and is mediated through the adrenal cortex. Grattan and Jensen (4) found that apparently only those principles of the adrenal cortex substituted in ring 3 (ketO- or hydroxy- group) are capable of inhibiting insulin hypogly cemia. This latter finding is in agreement with the observations of various other investigators (5–9) that apparently only those adrenal cortical principles, which contain either a ketc or hydroxygroup at Cn exert a significant influence on carbohy drate metabolism. Grattan and Jensen (4) suggested that the anti-insulin response produced by the adrenocorticotropic hormone and the corticosterone-like principles is probably due to the ability of these substances to induce the formation of glucose from non-carbohydrate sources with its subsequent deposition as liver glycogen.