METABOLISM, NUTRITION AND DIETETICS 521 



ing, and thus lead to the condition known as diabetic coma. The 

 small amount of carbon dioxide in the venous blood may also be 

 partly due to the hyperpnoea, marked by increased depth of the 

 respiratory movements produced by stimulation of the respira- 

 tory centre by other substances than carbon dioxide. The 

 increased ventilation causes a fall in the carbon dioxide pressure 

 in the alveolar air, and therefore an increased elimination of that 

 gas from the blood. This form of coma appears to be really in 

 part an acid-poisoning comparable to the condition produced in 

 animals by doses of mineral acids too large to be neutralized by 

 the ammonia split off from the proteins. The administration of 

 very large doses of alkalies (sodium bicarbonate, for instance, 

 to the amount even of hundreds of grammes) has been recom- 

 mended for the treatment of this serious complication, and in 

 many cases it is successful in staving it off for a time. Often, 

 however, in spite of a prolonged course of treatment, during 

 which the urine has continued distinctly alkaline, fatal coma 

 eventually occurs. The coma then is not merely a symptom of 

 acidosis, but is also due to the specific toxic effects of the acids 

 even when neutralized. Other toxic products may also be 

 formed in the deranged metabolism. 



Glycosuria can be caused in many other ways than those 

 already mentioned e.g., by concussion of the brain, occlusion 

 and subsequent release of the arteries supplying the brain and 

 cervical cord, acute haemorrhage, injection of water or physio- 

 logical salt solution into the bile-ducts, into the mesenteric 

 veins, or, in considerable amount, into the general circulation. 

 Carbon monoxide has a similar action owing to the deficiency of 

 oxygen occasioned by it. Many drugs also cause glycosuria, 

 including curara, morphine, phloridzin, adrenalin, and other 

 substances. Of these the last two are the most interesting. 



Phloridzin glycosuria agrees with pancreatic, but differs 

 from ' puncture ' 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 phloridzin acts on the kidney in such a way as to in- 

 crease the permeability of the glomerular 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 addition, within 

 certain limits there is a total inability on the part of the body 

 to consume dextrose. 



