Mis PHYSIOLOGY CUM'. 



excision intermittent instead of persistent glycosuria has been 

 observed (Paderi) ; sometimes severe glycosnria occurs even with 

 partial excision (Sandmeyer). 



Many and various have been the hypotheses put forward to 

 explain the relation between loss of pancreas and diabetes. Some 

 of these can at once be set aside, on the strength of experimental 

 data. 



As we saw in considering the internal function of the pancreas 

 (see pp. 98-102), the genesis of pancreatic diabetes was at first 

 explained by the serious disorder of the intestinal processes that 

 occur after loss of the digestive functions of the pancreatic enzymes. 

 De Dominicis ascribed the pancreatic diabetes to an auto-intoxica- 

 tion due to the absorption of abnormal substances developed in the 

 intestine, after suppression of the various functions of the pan- 

 creatic juice. Gaglio, in support of this notion, added that the 

 toxin which causes the diabetes penetrated from the intestine to 

 the blood, by the lymphatics. 



This hypothesis was, however, contradicted by the fact that a 

 segment of pancreas isolated from the intestine and from the 

 abdominal cavity (Minkowski, Hedon, U. Lombroso), or excreting 

 outside the body (Minkowski, Burkhardt, U. Lombroso), sufficed 

 to check the development of diabetes. It is thus necessary to 

 admit that the pancreas, besides its office of secreting digestive 

 juice, is the seat of an internal function, by which the formation 

 or consumption of glucose is regulated (see pp. 98-102). 



Others suppose that a toxic substance capable of producing 

 diabetes is continually formed in the body, and is normally 

 destroyed by the pancreas as fast as it is formed. After removal 

 of the pancreas, diabetes would develop by a kind of auto-intoxica- 

 tion, analogous to that which occurs after thyroidectoniy. But 

 this hypothesis has been experimentally proved fallacious. It was 

 demonstrated first by von Mering and Miukowski, and subsequently 

 by Hedon, that intravenous injection of blood from a diabetic dog 

 neither produces glycosuria in a normal animal, nor increases it if 

 present after loss of the pancreas. 



A. and E. Cavazzani, who, as we have seen, discovered nerve 

 fibres to the liver in the caeliac plexus, which, on excitation, pro- 

 mote hepatic glycogenesis, suggested that the diabetes consequent 

 on excision of the pancreas is due to the operative act in which 

 these nerves, which regulate the production of glucose in the liver, 

 are injured. In fact, they described lesions both of certain cells in 

 the caeliac plexus and of the hepatic cells in depancreatised animals. 

 They were thus led to assume an analogy between pancreatic 

 diabetes and Bernard's paralytic secretion of saliva, taking both to 

 be the effect of a degenerative irritation of the secretory nerves. 

 Several data, however, tell against this hypothesis. It is possible 

 to excise a large part of the pancreas without inducing true 



