RECENT chemical studies, during the treatment of diabetic acidosis, have emphasized certain changes in electrolyte balance which warrant careful appraisal and possible therapeutic application. Soon after the discovery of insulin, Harrop and Benedict (1), and shortly thereafter Briggs and co-workers (2), demonstrated a fall in the potassium level in the plasma when insulin was administered. In the early period after the introduction of insulin little attention was given to the fall of potassium following the administration of insulin, since the glycosuria, hyperglycemia and ketonuria were the factors deserving the greatest emphasis in the treatment of the diabetic state. In 1933 Atchley, Loeb and co-workers (3) noted electrolyte changes with a fall in plasma potassium in two diabetic patients upon withdrawal and then later reestablishment of insulin therapy. Shortly thereafter Elkinton and coworkers (4), and the Wileys (5) noted a fall in plasma potassium in states of diuresis and dehydration. This led to Darrow's (6) therapeutic regimen for replacing the large losses of potassium seen in the diarrheas of infancy. In 1937 when Bellet (7) noted the electrocardiographic changes during emergence from diabetic acidosis there was a revival of interest in electrolyte balance in diabetes. In 1946 Holler (8) reported a patient who was vigorously treated for diabetic acidosis, and developed a respiratory paralysis due to a critically low level of potassium in the plasma, with recovery after the administration of a solution of potassium. Critically low levels of potassium, during the period of treatment of diabetic acidosis, have also been reported by Martin and Wertmann (9), Nicholson and Branning (10), and Frankel and co-workers (11).