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The Effect of Excessive Dietary Sodium and Potassium on the Carbohydrate Metabolism of Normal Rats^1,2,

Two Figures

Department of Biochemistry, the University of Colorado School of Medicine, Denver

Male albino rats of the Yale strain were maintained for a period of 2 weeks on normal diets and on diets high in sodium or potassium. After this period determinations were made of the glucose tolerance, the response to insulin, the deposition of gycogen following the feeding of glucose or a measured amount of mixed diet, and the R. Q. in fasting animals and after the administration of glucose.

Whereas statistical analysis showed a significant difference in the values at only one point in the glucose tolerance curves, the curves of the animals fed excessive sodium tended to be lower than those of the control rats when 0.5 gm. of glucose per 100 gm. of body weight was given.

The animals which received excessive sodium were more sensitive and those which received excessive potassium were less sensitive to administered insulin than were those on a control diet.

When the liver glycogen was determined after a 24-hour fast there were no significant differences between the dietary groups. Following the administration of a measured dose of glucose the liver glycogen of the animals on excessive potassium was significantly lower than that of the control animals. Those which had received excessive sodium did not vary significantly from the controls under these conditions. However, when a standard feeding of mixed diet was given, the results showed a significant increase in liver glycogen storage by the animals receiving excessive sodium. The dietary regimes employed had no significant effect upon the muscle glycogen.

The increase of the R. Q. following the administration of glucose was neither as marked nor as prolonged in the animals which had received excessive sodium as it was in those on a control diet. The rats which had received excessive potassium did not vary significantly from the controls.

² Presented in part before the American Physiological Society, Chicago, Illinois, in April, 1941.

Manuscript received 29 April 1943.