STUDIES ON THE MECHANISM OF ALLOXAN DIABETES

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Abstract
Expts. in dogs and rabbits prove that the early alloxan hyperglycemia is not a causal factor in the development of alloxan diabetes. If a normal blood sugar is maintained by either insulin or phlorhizin for an initial period after the injection of alloxan, islet cell degeneration and diabetes will develop. Expts. on adrenalectomized rabbits show that the presence of an intact adrenal medulla is necessary for the initial alloxan hyperglycemia. Alloxan does not inhibit or inactivate insulin. The transitory alloxan hypoglycemia is produced by insulin liberated from the degenerating pancreatic islet cells. Depancreatized dogs and alloxan diabetic rabbits do not respond to alloxan with this characteristic lowering of the blood sugar. Alloxan exerts its diabetogenic effect by a direct action upon the pancreas. Bioassays of the pancreas of alloxan diabetic dogs show that the insulin content is markedly decreased. The diabetogenic action is a specific property of alloxan. Compounds like dialuric acid, alloxantin, violuric acid, barbituric acid, sodium nitroferri-cyanide, sodium molybdate, eeric sulfate, persulfate, quinone, quinoline, and cinchophen, were tested and failed to produce islet cell changes.

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