PATHOLOGICAL METABOLISM OF DIABETES 277 



and break upward abruptly. If the dialyzer contained a glucase instead 

 of u reuse and if glucose were added, the analogy would be complete. 



The pancreas is a gland innervated from the celiac plexus with vagus 

 and sympathetic fibers. If its function is to dispose glucose, more glucose 

 means more work to be done and more glucolytic secretion to be elaborated. 

 Glucose itself might be conceived as directly or indirectly stimulating this 

 nerve gland apparatus. Given an imperfect organ and an overburden 

 of glucose and fatigue or permanent injury might presumably result. Re- 

 lief from the overburden with rest for the apparatus would favor recupera- 

 tion to a degree. What originally weakens the apparatus in diabetes 

 mellitus ? 



The feeding of pancreas fresh or dried does not cure diabetes as 

 thyroid gland cures cretinism. The pancreatic hormone does not contain 

 iodin like that of the thyroid to indicate by a violet color whether it is 

 present or absent in an hydrolysis fraction. It would not be expected 

 to produce any immediately recognizable effect if injected into a normal 

 animal already containing it in excess. Unless Kleiner with a pancreas 

 emulsion has demonstrated an increased utilization of sugar, post mor- 

 tem in depancreatized dogs, no definite results have been attained with 

 pancreas preparations as yet. 



Acidosis 



The anomaly of the metabolism in which abnormal quantities of ace- 

 tone, acetoacetic and (3-hydroxybutyric acids appear in the tissues, blood 

 and urine, is not due directly to any impairment of the endocrin function, 

 of the pancreas. It is a secondary effect in the nature of a disturbed 

 metabolic balance resulting from the withdrawal of oxidizing glucose. 

 This anomaly is not peculiar to diabetes nor constantly associated with it. 

 It occurs in other diseases. It may be made to appear in a normal sub- 

 ject by starvation or a diet containing too low a proportion of carbohydrate 

 and too high a proportion of fat, and when this is done it may be made 

 to disappear again simply by the addition of more carbohydrate to the 

 diet. It appears to be the immediate result of the oxidation of certain 

 fatty acids in the absence of a sufficient proportion of "oxidizing" (dissoci- 

 ated) glucose. 



It would seem probable that for any given individual at any given time 

 there is a definite ratio between the quantity of glucose oxidizing in the 

 body and the maximum quantity of Jcetogenic acids that can be oxidized in 

 the same time without the appearance of abnormal amounts of the acetone 

 bodies. In other words, the quantity of oxidizing glucose fixes an upper 

 limit to the quantity of ket-ogenic acid that can be completely oxidized at 

 the same time. As to the absolute magnitude of this ratio and the degrees 

 of its variation in different individuals in health and disease, final state- 



