RELATIONSHIP OF THE ADRENAL GLANDS TO THE DIABETOGENIC EFFECT OF ETHYLENEDIAMINE IN THE PARTIALLY DEPANCREATIZED RAT

Abstract

These studies were designed to test the hypothesis that ethylenediamine causes exacerbation of diabetes in the partially depancreatized rat via activation of the anterior pituitary-adrenal cortex axis. Partially depancreatized male rats were force-fed a medium carbohydrate diet by stomach tube. Ethylenediamine was injd. in amts. of 0.05 ml. once daily for 5 days and twice daily for 5 days in each of 4 expts. In expt. 1, ethylenediamine was found to cause a rise in the level of blood glucose as well as in urinary glucose. In expt. 2, ethylenediamine caused exacerbation of the diabetes of adrenal demedullated rats. In expt. 3, moderately diabetic adrenalectomized rats treated with 3 glycogen units daily of adrenal cortical extract (ACE) failed to show exacerbation of the diabetes during the injn. of ethylenediamine. It was postulated that ethylenediamine (a noxious agent) may have an extra-adrenal diabetogenic action which is masked by the development of adrenal cortical insufficiency in rats on a fixed intake of ACE adequate to meet the needs of non-stressful conditions only. Expt. 4 was a partial test of this hypothesis. Very mildly diabetic adrenalectomized rats were treated with 5 glycogen units of ACE per day. The injn. of ethylenediamine caused exacerbation of the diabetes in each of the adrenalectomized rats but the response was greater in nonadrenalectomized animals. These expts. show that ethylenediamine has an extra-adrenal effect upon glycosuria but that the response is modified by removal of the adrenal glands. It is suggested that the secretory response of the adrenal cortices during the injn. of ethylenediamine tends to maintain a state of eucorticalism which is essential for biologic responsiveness.