GLYCOLYSIS 255 



might be proposed : that the liver itself is not actually in- 

 capable of building up glycogen in pancreatic diabetes, but 

 that an increased activity of the hepatic diastasic ferment 

 (normally kept in due bounds by the internal secretion of 

 the pancreas) makes it impossible that the glycogen be re- 

 tained. But apparently after extirpation of the pancreas 

 the amount of diastase in the blood undergoes reduction. 20 

 Statements indicating that the diastasic power of the liver 

 is increased in diabetes 21 are contradicted by other com- 

 pletely negative results. 22 So there is no outlet apparent 

 in this direction. 



Pfliiger noticed that in dogs with pancreatic diabetes, 

 with marked emaciation and their fat largely lost, the liver 

 in contrast with other organs had distinctly increased in 

 weight. This suggests that the hepatic function here is 

 not depressed, but that the organ really is working under 

 abnormal stress to form out of carbohydrate-free material 

 the large amounts of sugar which appear in the urine. Yet in 

 this connection it may be noted that in Embden's laboratory 

 in the artificially perfused liver of the depancreatized dog, 

 practically free of glycogen, the new formation of sugar 

 proved to be no greater than in an organ freed of its glycogen 

 by work or by strychnia convulsions. 23 



For the present, therefore, we possess no satisfactory 

 explanation for the mystery of pancreatic diabetes either 

 in the formation of glycogen in the liver, its diastasic power, 

 or in its ability to produce sugar from carbohydrate-free 

 material. 



Glycolysis. The hypothesis framed by Lepine seems 

 much more attractive. The pancreas is supposed by him 



20 W. Schlesinger (Vienna), Deutsch. med. Wochenschr., 1908, 593; L. K. 

 Goult and A. J. Carlson (Chicago), Amer. Jour, of Physiol., 29, 165, 1911. 



21 A. Hinselmann (Med. Clinic, Heidelberg), Zeitschr. f. physiol. Chem., 

 61, 265, 1909. 



22 1. Bang, Hofmeister's Beitr., 10, 320, 1907 ; F. A. Bainbridge and A. P. 

 Beddard, Biochem. Jour., 2, 89, 1907; cf. also O. J. Wynhausen (Amsterdam), 

 Berlin, klin. Wochenschr., 1910, 2107. 



23 L. Lattes, Biochem. Zeitschr., 20, 215, 1909. 



