366 INTERNAL SECRETIONS OF PANCREAS AND SPLEEN. 



section of the splanchnic nerves (centrifugal nerves) and of the 

 medulla above the origin of these nerves prevents both the 

 experimental diabetes of Claude Bernard and the toxic diabetes 

 caused by morphine." 



The list of drugs that are able to produce glycosuria could 

 be indefinitely prolonged: it includes all those that produce 

 suprarenal overactivity. But this does not mean that the fer- 

 ment-producing organ is alone stimulated; glycosuria is but 

 one of the manifestations of the exaggerated general metabo- 

 lism induced, and oxidation processes are enhanced accord- 

 ingly. Toxic glycosuria, therefore, only represents the sur- 

 plus of sugar which oxidation processes have not consumed;, 

 the excess of sugar actually produced is probably far greater 

 than the surplus which the urine shows. Again, certain drugs 

 phosphorus, for instance do not produce glycosuria to any 

 marked degree; as soon as the dose capable of causing it is 

 reached, the adrenals lapse into insufficiency, and, if the dose 

 is pushed to any extent, even the normal ratio is reduced. 

 Antipyrin is now considerably employed in diabetes; we have 

 seen that this drug and acetanilid readily produced suprarenal 

 insufficiency and dissociation of the haemoglobin molecule. 

 This is sufficiently extensive sometimes to manifest itself a& 

 methaemoglobinuria or even hgematoporphyrinuria. All these 

 facts seem to us to indicate that toxic glycosuria is primarily 

 due to over stimulation of the adrenal system, the excessive func- 

 tional activity which increased oxidation produces giving rise to an 

 inordinate production of an agency that converts glycogen into sugar. 

 All these features will again be reviewed. 



That the agency which converts glycogen into sugar is 

 the amylolytic ferment produced by the pancreas to which we 

 have referred is further sustained by the foregoing facts, espe- 

 cially in view of the amylolytic properties of the pancreatic 

 secretion in the intestine. Since the conversion into sugar 

 occurs during fasting as well as during digestion under the 

 effects of toxics, the reaction can only include the hepatic 

 glycogen and pancreatic ferment; and, there being nothing in 

 the intestine to convert during fasting, the ferment must nec- 

 essarily reach the glycogen by another channel. May this not 

 "be the more direct route afforded ly the splenic vein? 



