Irvine McQuarrie ai^j 



while it leaves the muscle or enters the liver along with lactic acid. Some sup- 

 port for such a tentative hypothesis is found in the observation that after 

 muscular activity there is a consistent increase in the K content of the liver." 

 The existence of a K cycle from muscle to liver and other viscera, and back 

 again, comparable to the lactic acid cycle of Soskin" and Cori'' is suggested. 

 In this connection it is interesting to refer briefly to studies on the K and 

 carbohydrate metabolism in the clinical condition known as familial periodic 

 paralysis. In this disorder serum K is found to be very low during periodic 

 attacks of muscular paralysis (Walker'"). Attacks are brought on by excessive 

 carbohydrate intake. Administration of K salts raises the serum K and causes 

 prompt relief of the paralysis (Aitken and co-workers"). Aitken and co-workers" 

 showed that paralytic attacks could be induced at will in such patients by any 

 procedure that lowers serum K. The K-lowering effect of glucose or levulose by 

 mouth or by vein was found to be more marked than in the normal subject. 

 Allott and McArdle'^ found by balance studies that K is retained by the body 

 during an attack. Phosphate was the only other inorganic substance found 

 to be altered in attacks. It tended to parallel changes in K. The disease, there- 

 fore, appears to involve the hexosephosphate mechanism in some manner. 



Antagonistic Effects of Na and K on Carbohydrate Metabolism 



The attention of the author and his associates (McQuarrie and co- workers*"' ^°) 

 was first directed to the possibility of an interrelationship between the Na and 

 K economy and carbohydrate metabolism in 1930, when they observed freakish 

 variations in the degiee of glycosuria shown by an 8-year-old diabetic girl, 

 who manifested an abnormal craving for salt. Although the patient was main- 

 tained on a uniform diet, it was found that the total amoiuit of sugar in the 

 urine for a given period tended to \ ary inversely with the quantity of NaCl 

 which she was allowed to consume. Unfortunately, an attempt to carry out a 

 more complete investigation of the observed phenomenon in that patient was 

 frustrated by her premature discharge from the hospital to move with her 

 parents to another community. 



Three years later, however, a second diabetic child, complaining of an 

 almost insatiable craving for salt, was subjected to a series of metabolic studies 

 originally designed primarily to determine the natm^e of the physiological 

 disturbance responsible for this bizarre symptom. This patient, a 15-year-old 

 boy, was found to require between 80 and 90 gm. of table salt daily to satisfy 

 his craving. Since he had been on an ordinary diabetic diet (naturally high in 

 K) for a long period of time, had partially depleted his reserve of fixed base 

 as a residt of a mild degree of diabetic acidosis and had vomited an undeter- 

 mined number of times just prior to his admission to the hospital (thereby 

 losing a considerable amotnit of chloride), the inordinate craving for salt was 

 at first presumed to be explainalile on the simple basis of temporary physio- 

 logical need for both Na and CI. That such an explanation was quite inade- 

 cjuate soon became apparent, however, when the craving was observed to 



