528 DIABETES 



acid, are formed. An important observation, in view of our 

 knowledge of the ability of pancreatectomized animals to utilize 

 levulose, is that the combined pancreas-muscle or pancreas-liver 

 extracts do not destroy levulose. 1 



The activating substance may be compared with the entero- 

 kinase of the intestine, which activates the inert trypsinogen of 

 the pancreatic juice ; and Cohnheim calls it the " pancreas acti- 

 vator." It acts in very small quantities, is not destroyed by 

 alcohol or by heating to boiling, and excessive quantities prevent 

 activation (similar to Ehrlich's "deviation of complement"). 

 Although numerous objections to Cohnheim's views have been 

 made, yet the main fact that the pancreas produces an activator 

 substance for a glycolytic enzyme contained in other tissues 

 seems to have been safely established. 2 



Defective GlycogenesiS. This discovery perhaps ex- 

 plains why the power to utilize sugar is reduced, but it does 

 not by any means explain all the features of diabetes following 

 pancreatic injury. One of the most important characteristics 

 of pancreatic diabetes is the almost complete disappearance of 

 glycogen from the liver, and, to a less extent, from the muscles, 

 while at the same time there may be a deposition of glycogen in 

 excessive quantities in other tissues where it does not normally 

 occur abundantly (see " Glycogenic Infiltration," page 363). 



This decrease in the glycogen of the liver occurs at a time 

 when the blood contains much more sugar than it does normally, 

 and indicates that the liver has almost entirely lost its normal 

 power of converting all excessive sugar into glycogen. On this 

 account we cannot be completely satisfied with an explanation 

 of pancreatic diabetes that accounts merely for decreased destruc- 

 tion of sugar, as does Cohnheim's pancreas activator. We must 

 also account for the impaired glycogenesis. v. Noorden seeks to 

 explain this defective formation of glycogen by the hypothesis 

 that the pancreas furnishes a secretion which either favors the 

 polymerization of sugar into glycogen, or else inhibits the 

 power of the tissues to split up the glycogen that they have 

 formed. Of the two possible errors, excessive destruction and 

 faulty formation of glycogen, he is inclined to favor the latter 

 as the more probable, in view of the well-known fact that pan- 

 createctomized dogs and diabetics can form glycogen out of 

 levulose, when they are unable to form it out of glucose. The 

 added fact that diabetics can frequently utilize levulose, in spite 

 of the fact that the glycogen so formed must later become glucose, 



1 Sehrt, Zeit. klin. Med., 1905 (56), 509. 



2 See Cohnheim's recent publication, Zeit. physiol. Chem., 1906 (47), 253. 



