316 PHYSIOLOGY CHAP. 



these data we may conclude that diabetics have to a large extent 

 lost the power of utilising dextrose and glucose. 



Since the greater part of the sugar formed in the body is 

 consumed by the muscles, which function under the influence of 

 the nervous system, it is natural to conjecture that the patho- 

 genesis of diabetes is to be found in a specific alteration of the 

 nervous system, more or less diffused in the centres. 



Bernard's so-called diabetic puncture, of which we have already 

 spoken, seemed at first sight to clear up the obscure pathogenesis 

 of diabetes mellitus. But the glycosuria due to puncture of the 

 fourth ventricle is quite transitory ; it ceases after a few hours, 

 and the liver remains almost free of crlycoen. Puncture does not 



O v O 



produce glycosuria in an animal deprived of its glycogen by fasting. 

 If glucose be injected into the meseuteric vein of an animal in 

 which the glycogen store in the liver has been exhausted by 

 fasting, but little sugar escapes with the urine, viz. only that 

 which the liver is unable to fix in the form of glycogen. If, on 

 the contrary, the glucose be injected into the mesenteric vein of 

 an animal that has suffered Bernard's puncture, almost the whole 

 of the sugar is eliminated by the kidneys (Naunyn). It is there- 

 fore clear that Bernard's so-called experimental diabetes is a process 

 fundamentally distinct from the true diabet'es mellitus, which, as 

 we have seen, does not depend on incapacity of the liver to form, 

 or to retain glycogen. 



Another form of temporary glycosuria is that which v. Mering 

 obtained in 1886 by means of phloridzin. This glucoside (which 

 is extracted from the root-bark of apple and cherry trees) on 

 boiling with acid breaks up into phloretin and dextrose. When 

 introduced into the stomach of dogs in a quantity of 1 grin, per 

 kilo, body-weight, a glycosuria lasting 2-3 days is produced after 

 a few hours. If the animal be killed after glycosuria has ceased, 

 the glycogen accumulated in both the liver and the muscles is 

 found to have entirely disappeared. So far the process seems to 

 be identical with that which ensues on Bernard's puncture : but 

 it differs essentially in that a second dose of phloridziu administered 

 to the animal after the effect of the first has worn off, regularly 

 reproduces the glycosuria. It is evident that the sugar produced 

 and eliminated after this second poisoning cannot originate in 

 dextrose formed by phloridzin decomposition nor from glycogen, 

 which no longer exists, but that it must come from other materials 

 present in the body, possibly from either the proteins or the fats. 

 The action of the liver does not seem to be necessary to the 

 production of phloridzin diabetes. It can in fact be produced in 

 the frog after removal of the liver. 



Minkowski maintains the hypothesis of the renal origin of 

 phloridzin diabetes, and assumes that the drug breaks up in the 

 kidneys into phloretin and glucose ; that the latter is eliminated, 



