STUDIES ON THE MECHANISM OF ALLOXAN DIABETES

Abstract

IN APRIL 1943 Shaw Dunn, Sheehan and McLetchie announced their discovery that alloxan, the ureide of mesoxalic acid, causes necrosis of the pancreatic islet cells. In the meantime, the diabetogenic action of alloxan has been demonstrated almost simultaneously by Dunn and his associates in Glasgow (1943), by Bailey and Bailey in Boston (1943), and by Goldner and Gomori in Chicago (1943). Alloxan diabetes has been produced in rats, rabbits, dogs, monkeys, and cats (Goldner and Gomori, 1944). Anatomically, this diabetes is characterized by the selective necrosis of the beta cells in the islets of Langerhans. Prior to the establishment of the diabetes, the blood sugar of alloxan treated animals shows a characteristic triphasic reaction, which was first observed by Jacobs in 1937. An immediate hyperglycemia which reaches its peak within two or three hours, is followed by a severe, often fatal hypoglycemia, which after a duration of several hours yields to the final hyperglycemia (Fig. 1).