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Depletion of the body stores of fixed base is the most serious complication of diabetic ketoacidosis, and losses of total body sodium of 25 to 50 per cent have been reported in diabetic acidosis in man (1-4). Recent work from several laboratories has indicated that from 30 to 45 per cent of the total body sodium exists out of solution in the mineral solids of the skeleton (5-7). It has also been demonstrated that this store of sodium is not fixed but may increase or decrease depending on whether the individual is subjected to excess sodium intake, uncompensated sodium loss or acidosis (8-10). The degree to which the bone sodium pool may be reduced seems to vary with the intensity and duration of the sodium loss and acidosis (7) and probably with the age of the animal (7, 8, 11). Therefore, experiments designed to examine effects of diabetes and of acidosis, separately and together, upon the size of this store of body sodium should be of value in designing rational electrolyte replacement therapy in diabetic acidosis. In the experiments reported here the bone sodium content of rats with alloxan diabetes of both short and long duration was compared with normal controls of equal age. In addition, normal and diabetic rats were rendered acidotic by the intraperitoneal injection of ammonium chloride and the response of their bone sodium to this stimulus was examined. The results indicated that untreated alloxan diabetes, in the absence of acidosis, as indicated by normal blood pH's, had no effect on bone sodium stores, and that both normal and diabetic animals responded to acidosis with a comparable decrease of about 12 per cent in bone crystal sodium content.

The Effect of Alloxan Diabetes and Acidosis on the Mineral and Water Content of Bone12