IT IS now well recognized that the phosphate cycle constitutes the mechanism whereby energy resulting from oxidation is rendered available to living cells.1A notable rise in the plasma level and urinary excretion of phosphorus has been found in diabetic acidosis.2This apparently causes a significant depletion of phosphorus stores in the body, as shown by the response to insulin. The plasma and urinary phosphorus levels fall precipitously and remain subnormal for as long as a week after institution of insulin therapy.2bThe fact that death may occur in circulatory collapse after abolition of ketosis, restoration of a normal blood sugar level and replacement of apparently adequate amounts of water and sodium chloride raises the question of the clinical importance of deficiency of other elements, notably phosphorus and potassium. One of the objectives of the present study was to determine the clinical efficacy of intravenously administered sodium