IT IS generally agreed that diabetic acidosis develops from excessive production of ketone in the body consequent on diminished glucose oxidation and depletion of liver glycogen. In order to check production of ketone, therapeutic efforts have been directed toward acceleration of glucose oxidation and restoration of liver glycogen. Soskin1 and Mirsky2 have found that the maintenance of considerable hyperglycemia through the intravenous injection of large amounts of dextrose accelerated glucose oxidation and glycogenesis in the liver and the disappearance of ketosis. For this reason it had been our custom to begin administration of dextrose early in the treatment of diabetic coma, while hyperglycemia was still present. However, the development of fatal circulatory collapse or cardiac failure during the course of therapy has led us to reevaluate the effects of early administration of large amounts of dextrose on the carbohydrate metabolism, acidosis, water balance and clinical course of diabetic