712 A. S. WARTHIN 



f 



mally going on in the gland. Pathologic exaggerations of these processes 

 may he found in the form of an essential atrophy of the organ. 



The workers who have busied themselves with anatomico-pathologic 

 changes in the pancreas in human and experimental diabetes may be 

 classed as follows : Those who attribute the external secretion to the acini, 

 and the internal secretion to the islands, and consider lesions of the latter 

 to be the cause of diabetes; those who attribute to lesions of the acini 

 the preponderating role in the genesis of diabetes; those who hold that 

 the internal secretion of the pancreas belongs to both acini and islets, 

 and that generalized lesions of the pancreas are by far the most common 

 findings in human diabetes. Lombroso is one of the chief representatives 

 of this group. The great majority of observers agree that the pancreas 

 is an organ of internal secretion (islets or acini alone, or both concerned) 

 which takes part in the regulation of sugar metabolism. That this sugar- 

 regulating function of the pancreas is not the only factor involved in the 

 normal regulation of the carbohydrate metabolism, but is only a link in a. 

 complicated chain involved in this metabolism seems most probable from 

 all of the evidence so far gained. Diabetes might, therefore, occur 

 as a result of a disturbance in some other member of this chain while 

 the internal function of the pancreas is normally produced. If it can- 

 not now be affirmed beyond doubt that all cases of diabetes are due to 

 pancreatic disease a certain number of them are definitely associated with 

 alterations of this island. 



Researches as to the Nature of tlie Internal Secretion of the Pancreas. 

 With the growing belief in the endocrinal function of the pancreas 

 experimental investigations became more and more concerned with at- 

 tempts to prove the existence and character of the hypothetical hormone. 

 The researches began to follow physiologic or biochemic lines rather 

 than anatomic. 



Pfliiger's idea of a duodenal diabetes" and of the nervous origin of 

 diabetes, as opposed to the internal secretion theory, had first to* be dis- 

 posed of. This investigator maintained that the pancreatic diabetes of von 

 Mering and Minkowski was really a duodenal diabetes, caused by the 

 destruction of nerves passing from anti-diabetic centers in the wall of the 

 duodenum. Ehrman, Lauwens, Rosenberg and Minkowski showed that 

 the total removal of the duodenum in the dog did not cause diabetes; 

 Pratt separated the pancreas from the duodenum without producing gly- 

 cosuria ; and Rosenberg showed that Pfliiger's duodenal diabetes in frogs 

 was a glycosuria due to exposure to cold, his frogs having been kept on 

 ice. Martina freed a portion of the pancreas from its vessels and nerves 

 and transplanted it into the spleen of a dog, which survived the extir- 

 pation of the remainder of the gland for three months in spite of the 

 development of a well-marked diabetes. This gave a firmer position for 

 the internal secretion theory as opposed to the neurogenic. Forschbach, 



