v INTERNAL RESTITUTIVE SECEETIONS 321 



consumption of the sugar which forms the principal source of 

 carbonic acid production. The glycolytic processes are thus 

 considerably reduced in intensity in pancreatic diabetes. 



Pfliiger, in his important monograph on Glycogen (1902-3), 

 maintained the exact opposite, and held that the hyperglycaemia 

 and glycosuria consequent on ablation of the pancreas depend not 

 on decreased glycolysis but on increased glycogenesis, in excess of 

 the limits within which the body is able to burn up the sugar 

 introduced into it, or which it forms. 



How this hyperglycogenesis takes place in depancreatised 

 animals is not very clear from Pfliiger's many publications on the 

 subject. For a long time he maintained that the amount of 

 sugar present in the urine of depancreatised dogs is never in excess 

 of that furnished by the glycogen stored up in the body, and 

 derived from alimentary carbohydrates. But after fresh experi- 

 ments undertaken in a controversy with Liithje, he convinced 

 himself of the necessity of admitting that glucose may arise from 

 other sources, particularly from the fats accumulated in the liver, 

 while on the other hand he excluded the alimentary proteins, for 

 which Liithje argued. Gerhardt had observed that much fat could be 

 extracted from the blood and liver of the dog during pancreatic 

 diabetes ; Pfliiger, after 16 days' pancreatic diabetes in a fasting 

 dog, observed an increase of weight in the liver owing to an 

 enormous amount of fat. It is thus probable, according to Pfliiger, 

 that in pancreatic diabetes the fat co-operates in sugar formation 

 to an amount so much in excess of that normally formed as to 

 produce elimination of the excess by the kidneys. 



In 1903, to explain the hyperglycogenesis in pancreatic diabetes, 

 Pfliiger invoked the existence in the pancreas of an anti-diastase 

 which normally moderates the action of the diastases of the liver 

 cells; in ablation of the pancreas the increase in glycogenesis 

 would result from the deficiency of an ti- diastase. In 1905, on 

 the contrary, he supported the theory of the nervous origin of 

 pancreatic diabetes, which he regards as a nerve reflex. 



In order to demonstrate that the oxidative processes are not 

 diminished in diabetics, Pfliiger cites the observations of certain 

 authors, according to which the elimination of C0 2 in diabetics is 

 equal to the amount normally eliminated (contrary to the positive 

 results of Colasanti and Bonanni on depancreatised dogs). This 

 argument does not, however, seem to us conclusive. The normal 

 animal is capable of burning up an enormous amount of alimentary 

 carbohydrate before glycosuria from insufficient glycolysis makes 

 its appearance. Depancreatised animals, on the contrary, do not 

 cease to eliminate sugar even during a prolonged fast until they 

 die from starvation. Obviously, therefore, the contention that 

 pancreatic diabetes is due to increased glycogenesis rather than to 

 decreased glycolysis has no value. Increased glycogenesis can only 



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