METABOLISM OF CARBO-HYDRATES GLYCOSURI AS 545 



dogs. And the derangement in the normal sequence of events, of 

 whatever nature it may be, is not so deep-reaching as to prevent 

 the retracing of the chemical steps by which sugar is synthesized 

 from such derivatives of the proteins as amino-acids or their further 

 degradation products. As to the actual cause of the alleged in- 

 capacity of the tissues to consume dextrose, the change has by some 

 been supposed to be the loss or diminution of a glycolytic ferment 

 or a substance necessary for the activation of such a ferment. And 

 although the sugar- destroying power of blood from diabetic patients, 

 or from animals in which glycosuria has been caused by phlorhizin, 

 is not at all inferior to that of healthy blood, it has been maintained 

 that the intracellular glycolytic ferments, if such really exist, are 

 much less active, especially in the more severe forms of the disease, 

 which conform so closely in their clinical manifestations to the pic- 

 ture presented by the depancreatized animal. Nevertheless, up to 

 the present all attempts to satisfactorily demonstrate for isolated 

 tissues a loss or even a diminution in the capacity to utilize dextrose 

 have broken down. In eviscerated dogs, for example that is, in 

 preparations consisting mainly of skeletal muscle it has been found 

 impossible to make out any deficiency as compared with normal 

 animals in the amount of dextrose disappearing in a given time 

 from the blood, even when the animals have been deprived of the 

 pancreas as long as a week before the experiment, and therefore 

 exhibit the condition of pancreatic diabetes in full intensity 

 (Macleod and Pearce). This conclusion has been confirmed for the 

 isolated heart -lung preparation. 



As regards the hypothesis that an increased production of sugar 

 from proteins, or it may be from fat, is the essential proximate cause 

 of the hyperglycaemia and the glycosuria, there is no good evidence 

 that this factor, acting by itself in the absence of a derangement of 

 the regulative influence of the glycogen store, and in the absence of 

 a derangement of the normal katabolism of dextrose, is ever respon- 

 sible for pathological diabetes. But a secondary overproduction 

 of sugar unquestionably occurs in many cases. The tissues, bathed 

 as they are in liquids rich in dextrose, are nevertheless starving for 

 sugar^if they cannot use what is offered to tLem, and the body 

 labours to avert the famine by increasing its production of sugar, 

 the sugar-forming tissues being stimulated to their task either 

 through nervous influences or by chemical messengers circulating 

 in the blood. 



In depancreatized dogs, and in dogs under the influence 

 of phlorhizin, glycerin, given by the mouth, causes an increase in 

 the excretion of sugar up to two or three times the original amount. 

 The giving of fat does not increase the amount of sugar excreted, 

 which, however, is increased by such substances as egg-yolk, which 

 contain lecithin. These should accordingly be avoided in cases in 



35 



