EXPERIMENTAL DIABETES 361 



leevulose disappears in its passage through the organism. Lactose 

 causes a slight rise in the dextrose excretion, and has also a feeble 

 proteid-sparing action. 



A single dose of phloridzin does not appreciably affect the 

 amount of glycog&n in the liver and muscles. The repeated 

 administration of phloridzin, however, causes the glycogen stored 

 in the liver and muscles almost to disappear. Thus Prausnitz ( 25 ) 

 found the liver of a dog which had been kept under phloridzin 

 for twelve days meanwhile receiving no food to be practically 

 glycogen free ; the muscles of the same dog contained 0-3 per 

 cent, of glycogen. In another similarly treated dog Oil 25 grm. 

 glycogen was obtained from the liver, and the muscles contained 

 2'0 per cent. The glycogen does not, therefore, become used up 

 so quickly as in pancreatic diabetes. 



Another important distinction between phloridzin and all 

 other forms of diabetes is with regard to the amount of sugar 

 in the blood. In eleven cats Pavy produced diabetes by injecting 

 phloridzin subcutaneously ; during the time that the maximal 

 glycosuria existed, samples of blood were removed, and the per- 

 centage of sugar in them determined. The average amount was 

 found to be 0-149 per cent. In six normal cats, the average was 

 found to be 0-088 per cent. Similar observations on rabbits 

 and dogs (Coolen and Kolisch) showed the same result, viz. little 

 difference from the normal, if anything a slight increase, but never 

 sufficient to cause hyperglycsemia. 



In other forms of diabetes, too, ablation of the kidneys or 

 ligature of the ureters causes the percentage of sugar in the blood 

 to rise markedly ; no rise, however, occurs under similar conditions 

 in phloridzin diabetes. 



From what has been detailed it will be obvious that the cause 

 of the glycosuria which follows phloridzin administration must 

 be quite different from that of the other forms of glycosuria. It 

 cannot be due to hyperglycsemia, and there is no marked disap- 

 pearance of glycogen as in the other forms. These facts led von 

 Mering to suppose that the glycosuria was due to the fact that 

 the kidney, as a result of the action of the phloridzin, had acquired 

 an increased permeability towards dextrose, so that the normal 

 sugar of the blood was drained into the urine. Minkowski still 

 further elaborated this hypothesis by supposing that the phloridzin 

 was picked up by the renal cells and decomposed in them into 



