ON THE MECHANISM OF ENHANCED DIABETES WITH INFLAMMATION

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Abstract
An acute pleural inflammation in a dog fails to alter its blood sugar. The presence of an acute inflammatory reaction in a dog, rendered diabetic by pancreatectomy, induces a rapid and marked elevation in the blood sugar level. The extent of local proteolysis at the site of an acute inflammation in a diabetic dog is considerably more pronounced than that found in a non-diabetic animal. This is indicated by a lower conc, of the total proteins and a correspondingly higher concentration of urea, non-protein nitrogen and amino acid nitrogen than is encountered in the exudative material of a non-diabetic animal. The enhanced protein metabolism in the inflamed area of a diabetic animal is correlated with a marked elevation in both exudate sugar and exudate lactic acid. Insulin adm. reduces not only the level of sugar and lactic acid in such diabetic exudates; but this substance diminishes as well the degree of local proteolysis. This fact supports the view that gluconeogenesis at the site of an acute inflammation in a diabetic animal originates from proteins through examination of the molecule. Enhanced local proteolysis in the inflamed area of a diabetic animal implies increased tissue damage. The cyto-logical picture of a diabetic exudate indicates that poly-morphonuclear leukocytes manifest pronounced signs of cellular injury when compared with similar cells derived from a normal exudate. The biochemical changes encountered in the exudate of a depancreatized dog are similarly reflected in its circulating blood. Besides an elevation in blood sugar level, there is also an increase in the blood concentration of non-protein nitrogen, urea and amino acid nitrogen. Studies after pancreatectomy or splenectomy, and a comparison of the relative glucose concs, in exudate and blood, indicate that the raised levels in carbohydrate and nitrogenous constituents of the systemic circulation are neither due to the diabetes per se nor to the operative procedure. The elevation in the levels of these substances is referable to an absorption from the area of acute inflammation which complicates the diabetic disorder. Insulin by inhibiting glucose formation in the inflamed area likewise prevents a rise in the blood stream of intermediary products of carbohydrate and protein metabolism. The available evidences support the view that the mechanism of enhanced diabetes with concomitant inflammation might well be referable primarily to an increased local proteolysis in the inflamed area, favoring a combined picture of increased tissue damage with a corresponding elevation in glucose formation; the glucose, in turn, gradually diffuses into the systemic circulation.