594 SYNTHESIS OF UKEA. [BOOK u. 



yet in the alimentary canal ; we have seen that pancreatic juice 

 may carry part of the proteids on which it acts beyond the stage 

 of albumose and peptone, and reduce that part into leucin, tyro- 

 sin, and other bodies. We do not know, as we have already 

 said, to what extent this more profound digestion by pancreatic 

 juice does actually take place in the living body ; it may under 

 certain circumstances take place to a very slight extent and 

 under others to a considerable extent. But in any case it illus- 

 trates the way in which a somewhat similar disruption of proteid 

 material, a disruption which may be broadly described as a split- 

 ting up of the proteid into a nitrogenous and a non-nitrogenous 

 moiety, may take place somewhere in the body and so lead to 

 the sudden formation of some antecedent of urea. The ante- 

 cedent may be leucin or may be some other body or bodies. 



In support of this view may be urged the fact that such 

 bodies as leucin, glycin, asparagin and many others when intro- 

 duced into the alimentary canal are transformed into urea. 

 When these bodies are administered in not too great quantities 

 they do not reappear in the urine but the urea is proportion- 

 ately increased. 



J386. We have seen reason to think that proteids of a 

 are absorbed not by the lacteals but by . the portal blood 

 vessels, and such bodies as leucin probably take the same course. 

 This being so, all these bodies pass through the liver and are 

 subjected to such influences as may be exerted by the hepatic 

 cells. Now we have no positive evidence that the liver does or 

 can exert such an action on proteid material itself as to sepa- 

 rate a relatively simple nitrogen compound from the remaining 

 constituents, leaving these to form a body rich in carbon; we 

 have no positive proof that the increase of proteid metabolism 

 just spoken of as leading tc an increase of urea takes place in 

 the liver rather than in the- tissues at large; we may perhaps 

 suspect that it is so but we have no convincing demonstration. 

 We have however a convergence of evidence that the last stage 

 of the process, namely the conversion into urea of some or other 

 product of proteid metabolism which though allied to is not 

 exactly urea does occur in the liver. In the first place, a large 

 quantity of urea seems to be present in the liver of mammals; 

 in this respect the liver presents a strong contrast to the mus- 

 cles; in the liver of birds the urea is represented by urates. 

 In the second place, in certain cases of a form of disease of the 

 liver known as acute yellow atrophy in which the hepatic cells 

 are so changed that their functional activity is largely dimin- 

 ished, the urea of the urine not only undergoes a very marked 

 decrease but appears to be replaced to a very large extent by 

 leucin. This fact suggests that leucin (and not for instance 

 kreatin) is the chief immediate product of the nitrogenous 

 metabolism of the body, and that the leucin thus produced is 



