LNTEODUCTION 13 



however, are not conclusive. The glycosuria and other diabetic symptoms 

 that result from the extirpation of the pancreas might be due to the ac- 

 cumulation of toxins or metabolites in the blood, which, in the normal 

 animal, are removed or destroyed by the pancreas. This objection, how- 

 ever, cannot be offered to the observations of Hedon and of Carlson, 

 that transfusion of blood from the pancreatic vein of a normal animal 

 into the general circulation of a diabetic results in a diminution of the 

 glycosuria characteristic of the condition. On the other hand, the objec- 

 tion has been offered that such reduction might be due merely to ill-defined 

 "depressive" action of the foreign Hood. 



One of the most satisfactory demonstrations of the presence of a 

 hormone in efferent blood may be obtained by the so-called "crucial test" 

 of the production of secretin when acid is placed in the duodenum and the 

 duodenal venous blood shunted directly to the denervated pancreas. The 

 prompt appearance of augmented secretion in that gland would seem to 

 constitute indubitable proof of the presence of secretin in the blood. 



Another indirect physiological proof of the existence of a hormone in 

 the blood has been stressed by Gley (1917). This is the observation re- 

 corded by Miranoff that the denervated mammary glands of a female goat 

 hypertrophied during pregnancy and later secreted in a normal way. 

 Similarly, transplanted mammary glands have been shown to go through 

 the normal hypertrophic and secretory cycle during and following preg- 

 nancy. Such glands are supposedly free from the influence of any normal 

 nerve impulses and are hence amenable only to chemical influences. 



Such experiments are obviously open to the same objection as was 

 mentioned in the case of the pancreas. The hyperplasia may conceivably 

 be due merely to removal from the blood stream of some inhibitory sub- 

 stance which, in the non-pregnant state, holds the mammary tissues in an 

 inactive condition. Granting the existence of the assumed hormone lead- 

 ing to mammary hyperplasia, its source remains still unknown. It has 

 been ascribed by various investigators to the placenta and by others to 

 the fetus in utero. Support is lent to the latter hypothesis by the experi- 

 ments of Lane-Clapon and Starling and of Foa. These observers noted 

 mammary hyperplasia following injections of extracts of macerated 

 fetuses. Frank, however, has failed to confirm the observations and has 

 stressed the difficulty inherent in the marked variability of the normal 

 mammary glands, even in virgin animals. 



Other data bearing upon the topic under discussion will be found in 

 subsequent paragraphs under the caption "Methods of Experimentation." 

 At this point, however, it should be emphasized that despite a vast amount 

 of experimentation, we are still much farther from a logical proof of the 

 existence of numerous assumed hormones than is generally recognized. In 

 case of the thyroid and suprarenal glands only have Gley's three con- 

 ditions been met. Moreover, even in case of the suprarenal, concerning 



