Sodium and Potassium Salts in the Treatment of Experimental Diabetes and Diabetes Mellitus

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Abstract
Our experiments on human subjects indicate that there is no constant response to the ingestion of sodium chloride which warrants a conclusion as to its therapeutic value in diabetes mellitus. Limited experiments with potassium likewise gave inconclusive results. In some patients an apparent change in carbohydrate metabolism following the ingestion of sodium or of potassium is suggested, but this phenomenon is not sufficiently constant to justify any sound conclusions. Studies on diabetic animals definitely show that ingestion of sodium chloride or of potassium chloride may be followed by changes in sugar excretion of such magnitude as to suggest causal relationship. However, these changes are not constant. In the same animal, under experimental conditions identical as far as can be determined, the ingestion of sodium chloride is followed at one time by diminished glycosuria and at another time by increased glycosuria. Contrasting experiments on two dogs, the same paradoxical results are noted. Detailed analyses of our tables indicate that in some instances the results are more apparent than real and may actually represent coincidental changes in status. Our results do not entirely agree with those reported by McQuarrie, Thompson and Anderson. Differences in conditions of the experiments may to some extent account for this. Their experiments were conducted on children to whom they gave very large doses (60 to 90 gm.) of salt; most of our work was done on adult diabetics or on the depancreatized animal, and we were unable to employ the large salt dosage used by McQuarrie et al., without producing nausea, vomiting, or diarrhea. The most convincing experiment published by them concerned a salt craver who showed definite decrease in sugar output when sodium chloride was given. In no other case are their results as conclusive: the change in sugar output following the ingestion of sodium chloride or of potassium chloride suggests causal relationship, but may also be interpreted as a change in status of the patient. The possibilities of such changes influencing conclusions from therapeutic experiments in diabetes are explored and extended in our discussion of figure 1. The experiments on the goat seem of particular interest in that large changes in mineral equilibrium were produced by our experiments without demonstrable corresponding changes in sugar metabolism. It is probable that changes in cellular and tissue metabolism not elucidated by our protocols may explain the results. Our human and animal studies suggest one conclusion: changes in carbohydrate metabolism which follow ingestion of sodium or potassium chloride cannot be explained as a result of the mere addition of these salts to the dietary intake.

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