366 THE METABOLISM OF THE CARBOHYDRATES 



What, then, causes the hyperglycaemia in D. mellitus ? Can it 

 be due to an overproduction of sugar by the liver ? No doubt, as 

 we have seen, such is the cause of the transitory glycosuria which 

 sometimes accompanies injuries to nerves, or neuralgias, or the 

 presence of intracranial tumours ; but it cannot be the cause of the 

 glycosuria in the severer disease, else would we expect to find 

 entire absence of hepatic glycogen after death, and a disappear- 

 ance of the glycosuria after the store of glycogen had become used 

 up. Neither of these conditions has been shown to exist in 

 D. mellitus. The glycosuria persists till death ; and in the few 

 cases in which the liver has been examined for glycogen, some 

 glycogen has always been found, even although, in most of the 

 cases reported, the liver was not examined till some time after 

 death, so that post-mortem hydrolysis of glycogen might have 

 occurred. The histological examination of some liver cells from 

 two diabetics, removed by puncture of the liver with a trochar 

 during life, showed distinct glycogen masses in one case but only 

 small amounts in another case (Bunge, 8 p. 432). 



Some forms of temporary glycosuria, such as the so-called 

 alimentary glycosuria, may be due to inefficiency in the glycogenic 

 function of the liver to a sluggishness in the process so that 

 the excess of sugar in the portal blood during digestion is not 

 sufficiently retained by the liver, as a result of which some of it 

 passes into the systemic blood and induces hyperglycaBmia. It 

 is only after taking considerable quantities of sugar (100-200 grm. 

 dextrose) that glycosuria follows in this mild form of diabetes. 

 Starches do not cause it, for they are more gradually absorbed 

 and do not so markedly raise the sugar percentage in the blood 

 that leakage through the kidney filter should occur. The sugar 

 appears in the urine in from f-1 hr. after its ingestion. None of 

 the severer symptoms of diabetes is exhibited. 



By a process of elimination, then, we see that a want of de- 

 struction of dextrose in the organism must be the cause of the 

 glycosuria. Diabetes mellitus in man must be very similar, in its 

 chemical pathology, to pancreatic diabetes in animals, and indeed, 

 as we have seen, morbid changes in the pancreas are not infre- 

 quently found in patients dead of this disease. 



What direct evidence have we that in D. mellitus in man the 

 power of dextrose destruction in the body has been depressed ? 

 The answer to this question is furnished by administering dextrose 



