T26 FRANCIS H. McCRUDDEN 



(3) Glycosuria followed in five out of nine cases. 



A similar delay in glucose utilization has been observed by Janney and 

 Isaacson (6) accompanying the hypoglycemia in thyroidectomized dogs. 

 And Rosenthal(6) has observed that hypoglycemia accompanies diphtheria 

 toxemia in rabbits, except following administration of glucose, when a 

 hyperglycemia greater than that possible in normal animals occurs. The 

 liver and other organs appear unable to change the sugar to glycogen in 

 the normal manner. 



Impaired Glycogenesis. Hypoglycemia can be brought about by a 

 lowered threshold value for excretion of glucose through the kidneys 

 renal diabetes. Thus the sugar content of the blood can be lowered by the 

 administration of phlorizin, a drug which increases the permeability of the 

 kidney for glucose and causes glycosuria. The absence of glycosuria in 

 cases of progressive muscular dystrophy excludes this as a possible cause 

 of the hypoglycemia ( McCrudden (#), McCrudden and Sargent (a) (6) ). 



As glucose passes from the blood into the muscles and other tissues 

 where it is to be oxidized, the loss is made good from the glycogen store 

 of the liver. Replenishment is rapid and quantitative, the blood sugar 

 being thereby maintained at a fixed level. Hypoglycemia can result only 

 from a failure of replenishment to keep pace with the needs, a loss of 

 balance between supply and demand. 



Increased needs may result from increased sugar utilization or from 

 loss through the kidneys renal diabetes. In progressive muscular dys- 

 trophy we can rule out both. There is neither the rise in temperature 

 nor the increase in heat loss that would accompany increased sugar catab- 

 olism ( McCrudden (gr)). And the fact that the urine is sugar free 

 (McCrudden and Sargent (a) (6)) rules out renal diabetes. 



It has been pointed out earlier in this article that all forms of experi- 

 mental hypoglycemia are accompanied by an impairment in the glyco- 

 gen forming capacity of the liver and muscles. In these cases the glyco- 

 gen content of the liver and muscles is much below normal. It seems prob- 

 able that the immediate cause of the hypoglycemia is to be looked for in 

 a decreased rate of replenishment, consequent on the diminished glycogen 

 reserve. 



The possibility that the hypoglycemia in progressive muscular dys- 

 trophy might be due to impairment of the glycogen-storing power, led Mc- 

 Crudden and Sargent (a) to determine the glucose content of the blood in 

 one of these cases after a short period of starvation. Normally, as fast 

 as the glucose of the blood disappears, a continuous new supply, resulting 

 from the glycogenolysis, maintains the blood glucose at its normal level; 

 starvation has but little effect. Any interference with glycogen stor- 

 age might become apparent by a fall of the glucose content of the blood 

 after a short period of starvation. The patient went without food from 6 

 P. M. one evening until noon the next day, when the blood was taken 



