544 METABOLISM, NUTRITION AND DIETETICS 



reason to believe that diabetes mellitus is not a single pathological 

 condition, but comprises a group of such conditions. Some cases 

 present a picture conforming closely to one or to another of the 

 experimental glycosurias, but many cases a picture compounded of 

 features characteristic of two or of several of these experimental 

 conditions. 



It is possible that in some cases the sugar coming from the ali- 

 mentary canal passes entirely or in too large amount through the 

 liver, owing to a deficiency in its power of forming glycogen. But 

 although in certain cases of diabetes specimens of the hepatic cells, 

 obtained by plunging a trocar into the liver, have been found free 

 from glycogen, in others glycogen has been present. The muscles 

 also are usually stated to be much poorer in glycogen than normal 

 muscles, but this might just as well be the case because glycogen 

 was being transformed into sugar with abnormal ease as because 

 there was interference with glycogen formation. Indeed, it is said 

 that in the heart muscle of depancreatized dogs there is more glyco- 

 gen than in normal heart muscle. It must be carefully remembered 

 that the amount of glycogen present in a tissue gives no information 

 as to the rate at which it is being formed or decomposed. And if 

 the cause of the supposed defect in glycogen-forming power be the 

 absence of a glycogen-forming ferment, or its production in too small 

 an amount, the same circumstance may occasion a too tardy trans- 

 formation into sugar of whatever glycogen happens to be present. 

 In this case the sugar-regulating function of the glycogen store 

 would be equally lost, whether the storehouses were permanently 

 filled with long-formed glycogen or only half-filled or empty. 



In addition to an interference with the due and regulated storage 

 of the surplus sugar as glycogen, it has usually been thought neces- 

 sary for a rational explanation of the facts of diabetes, or at least 

 of some forms of it, to assume that from some change in the tissues 

 sugar has ceased to be a food for them, or is used up in smaller 

 amount than in the healthy body. 



Why the tissues cannot decompose and utilize dextrose as they 

 normally do, if it be really the case that they fail in this regard, is a 

 question of great interest, but as yet no satisfactory answer can 

 be given. It appears probable that the failure occurs at one or more 

 of the earliest stages in the intermediate metabolism of carbo- 

 hydrates (p. 534) or in the preliminary processes, whatever they 

 may be, which, without profoundly altering the dextrose molecule, 

 prepare it for the series of decompositions, in the course of which it 

 eventually parts with all its chemical energy. For it has been 

 shown that many of the products of the cleavage or oxidation of 

 sugar, even those in which the decomposition has proceeded but a 

 little way e.g., glyconic and glycuronic acids (p. 535) are com- 

 pletely utilized by the tissues of diabetics and of depancreatized 



