METABOLISM OF CARBO-HYDRATES-GLYCOSURIAS 551 



Fhlorhizin Glycosuria, produced by subcutaneous injection of the 

 glucoside phlorhizin, agrees with pancreatic, but differs from punc- 

 ture diabetes in this, that it can be produced in an animal free 

 from glycogen, and is accompanied by extensive destruction of 

 proteins. It differs from other forms of diabetes in being associated, 

 not with an increase, but with a diminution, in the sugar of the blood. 

 This is best explained by supposing that the phlorhizin acts on the 

 kidney in such a way as to increase the permeability of the glomeru- 

 lar epithelium for sugar, or (in terms of the secretion theory of urine 

 formation) in such a way as to increase its sensitiveness to the 

 stimulus of sugar circulating in the blood. The sugar is therefore 

 rapidly swept out of the circulation, and this leads secondarily to 

 an increased production of sugar to make good the loss. In addi- 

 tion, within certain limits there is a total inability on the part of 

 the body to consume dextrose. 



After the preliminary sweeping out of the sugar already in the 

 body, a definite ratio is established between the dextrose and the 

 nitrogen eliminated in the urine (dextrose : nitrogen : : 3~6or 37 : i). 

 The sugar at this stage is produced entirely from proteins, and not 

 at all from fat. It is a fact of considerable interest that, if small 

 quantities of dextrose are now given, the amount of protein de- 

 stroyed is reduced to some extent, although all of the dextrose is 

 excreted, and none of it is burnt (Ringer). This supports the 

 hypothesis of Landergren that in starvation some of the protein is 

 metabolized for the formation of the indispensable dextrose, and 

 that this fraction can be ' spared ' by carbohydrate, though not by 

 fat. The protein metabolized is so much increased under the 

 influence of phlorhizin that it exceeds the starvation requirement 

 by a greater amount than in pancreatic diabetes, perhaps because 

 the diminished content of sugar in the blood constitutes a more 

 insistent call upon the proteins to produce sugar. In pancreatic 

 diabetes, where hyper glycsemia exists, there can at least be no 

 reason for the formation of sugar from protein for the maintenance 

 of the normal sugar-content of the blood, and it is interesting that 

 in this condition the giving of dextrose does not seem to spare any 

 protein (p. 606). The degree of intolerance for carbo-hydrates in 

 pathological diabetes may be arrived at by putting the patient on 

 a diet of protein and fat (rich cream, meat, butter, and eggs), and 

 determining the ratio of dextrose to nitrogen excreted. If it as 

 3-6 or 3-7: i, intolerance is complete, none of the dextrose produced 

 from protein being burned (Lusk and Mandel). 



Glycosuria can be caused in many other ways than those already 

 mentioned. Sometimes the action seems to be a direct one on the 

 sugar-regulating centre e.g., in concussion of the brain, occlusion 

 and subsequent release of the arteries supplying the brain and 

 cervical cord, and acute haemorrhage. Carbon monoxide has a 



