EXPERIMENTAL DIABETES 357 



marked power in this direction. The extracts, however, do not 

 contain any amylopsin. The further results of their investigations 

 have not yet been published. 



To sum up, then, we see that the two most remarkable per- 

 versions of metabolism in depancreated animals are the disappear- 

 ance of glycogen from the tissues (liver especially) and the loss 

 of the power of oxidising glucose ; laevulose, however, can still 

 be oxidised and likewise form glycogen. 1 



Phloridzin Diabetes. In a series of papers, published between 

 1886 and 1889, von Mering described the course of the diabetes 



1 The explanation usually offered of this disappearance of glycogen from the 

 liver in pancreatic diabetes is as follows : the tissues have to a large extent lost the 

 power of oxidising dextrose ; this oxidation is, however, necessary for life, and, in 

 order that the organism may obtain more dextrose, the glycogen stored in the liver 

 and elsewhere is called upon, and in this way becomes uselessly used up in the 

 attempt of the tissues to try to oxidise sufficient dextrose by working on an excess 

 of it. In the case of laevulose, on the other hand, the co-operation of the pancreas 

 is not necessary for its oxidation ; some of it is immediately oxidised, and what 

 remains is converted into glycogen, which is only slowly converted into dextrose. 



Such an explanation is unreasonable ; it assumes that the remaining oxida- 

 tive power of the organism (see p. 368) can be forced to greater activity by pre- 

 senting a large excess of dextrose to the tissue cells, which presupposes that these 

 cells are not already dealing with as much dextrose as they can under the 

 circumstances that their remaining powers are not being exercised to the full 

 extent an assumption for which there is not a particle of evidence ; if it were the 

 true explanation, then we should expect that where the organism is offered 

 excess of carbohydrates if, in other words, the excess of dextrose which, accord- 

 ing to the theory, the tissues desire to have at their disposal, be increased from 

 without the glycogen would be saved, and could be found jn the liver, which, as 

 we have seen, is not the case. Is it not more probable that the internal secre- 

 tion of the pancreas normally acts on dextrose in some way so as to render it 

 capable both of oxidation and of transformation into glycogen ? in other words, 

 that as dextrose passes through the liver it is acted on by some ferment the 

 zymogen portion of which is derived from the liver, the activating portion from 

 the pancreas, or vice versa which changes it in some way so as to render it capable 

 of being oxidised, or, if not immediately required by the organism, of being stored 

 away as glycogen. Chauveau and Kaufmann have indeed claimed that the pro- 

 duction of sugar by the liver is controlled by an internal secretion from the 

 pancreas ; that normally this secretion inhibits sugar formation, so that when it is 

 removed, the latter process becomes excessive, and glycaemia and glycosuria are 

 the results. Markuse states that when the pancreas alone is excised in frogs 

 diabetes results, but that there is no diabetes when both liver and pancreas are 

 extirpated, and Montuori, that the same follows if the hepatic vessels be ligatured 

 in depancreated dogs. Kausch found that although pancreatic extirpation in 

 herbivorous birds did not cause diabetes it rendered the liver incapable of 

 forming glycogen. 



