422 Relation o£ Salts to Carbohydrate Metabolism 



They found that this loss of NaCl intensified the diabetes caused by removal 

 of the pancreas. Glycosuria and the fasting blood sugar were significantly 

 reduced, however, if NaCl was administered either with or without insulin 

 therapy. In several human diabetics tested by these authors, giving of extra 

 NaCl by mouth in moderate amounts (without regard to the K content of the 

 diet) did not appear to modify carbohydrate tolerance so definitely. 



Calculations based upon carbohydrate intake, decrease in glucose lost in 

 the urine, alterations in blood-sugar level and changes in volttme of body 

 fluids, indicated clearly that the diabetic patients studied by the author and 

 his associates (McQuarrie and co-workers'^") stored glycogen while ingesting 

 large amounts of NaCl. Direct proof that this type of regimen has such an effect, 

 at least in normal animals, was later furnished by the experiments of Crabtree 

 and Longwell."" These authors demonstrated a marked increase in the amount 

 of glycogen in the livers of young rats following ingestion by the latter of ex- 

 cessive quantities of NaCl. Anderson, Herring and Joseph,"^ in a study of the 

 carbohydrate stores in adrenalectomized rats given various amounts of NaCl, 

 found that such rats given 650 to 940 mg. NaCl daily for a period of 176 

 days after operation were able to store fed glucose almost as well as the normal 

 rat subjected to "sham adrenalectomy." However, animals fed amounts of 

 NaCl distinctly above or below this level were not able to do so. Glycogen 

 stores were lessened in animals given tap water instead of 1 per cent NaCl. 

 Excessive amounts of NaCl (1 234 mg. per day) prevented high glycogen storage. 



As regards the specific effects of intravenous KCl on the carbohydrate me- 

 tabolism of normal animals, results of various investigators have differed some- 

 what. Semler" early reported finding a sustained hyperglycemia after injection 

 of 3 to 5 gm. of this salt in diabetics. Kiyohara and co-workers'^ obtained 

 similar results from intravenous administration of KCl solution. Kylin and 

 EngeF" reported a slight initial decrease in blood sugar, but did not follow 

 the changes beyond one hour. In the rabbit, Odashima"' found blood sugar 

 to be lowered and lactic acid to be increased. More recently Silvette and Brit- 

 j.Qj^e7,6s reported the production of prolonged hyperglycemia and marked re- 

 duction in liver glycogen in normal rats following injection of KCl solution. 



Lewis*" found that excessive ingestion of NaCl increased, while KCl de- 

 creased, the sensitivity of normal rats to insulin. Animals with a high KCl 

 intake stored less glycogen following dextrose administration than control 

 rats. Those with an excessive intake of NaCl stored more glycogen but oxidized 

 less than control animals. Fasting blood-sugar levels and the carbohydrate 

 tolerance of normal rats were not found to be altered significantly by these 

 salts. In partially depancreatized, diabetic rats and in rats of the Yale strain 

 with hereditary diabetes, Orten and Devlin'"' '"demonstrated that carbohydrate 

 tolerance could be restored to essentially normal levels by the administration 

 of NaCl in large amounts without insulin. Sayers and Orten" found an in- 

 creased storage of glycogen in the livers of such diabetic rats after periods of 

 high NaCl intake. 



