NUTRITION 265 



the tissues. A certain fraction of the amino-acids must be supposed to escape the 

 action of the liver, in order to afford the nitrogen required by the tissues for 

 growth and maintenance. 



There are, however, certain difficulties in this view. In the first place, although 

 these acids in de-amination lose very little energy (see the work of Leathes, 1906, 

 p. 154), so that, as far as their actual content of energy is concerned, the fatty 

 acids are very nearly as valuable, yet there must be for this purpose alone some 

 way in which, as it appears, the amino-acids are superior to the simple hydrocarbon 

 acids. The taking of protein food causes a greater increase in the total metabolism 

 than a corresponding number of calories taken as fat or carbohydrate. This is 

 sometimes spoken of as the " specific dynamic energy " of Rubner. It seems 

 possible that the products of the de-amination reaction are more available in the 

 course of the reaction itself, that is, in the " nascent " state. For this reason, it 

 appears to be of advantage that the de-amination reaction should take place in the 

 tissue cells generally, and the ammonia sent on to the liver for conversion to urea. 

 The small amount of energy given off in de-amination would also be available. At 

 the same time, too much stress must not be laid on this point of view, since the 

 chief use of nitrogen food is to repair waste of tissue and not to supply energy, and 

 the actual amount demanded by the adult animal is not great. 



With regard to the "specific dynamic action " of proteins, Williams, Riche, and Lusk (1912, 

 p. 374) hold that the effect is due to the large influx of amino-acids causing increased metabolism 

 by their mass action on the cell protoplasm and that the view of Rubner does not explain the 

 facts, nor does that of increased intestinal activity. 



In the second place, certain experiments tend to show that the liver has not 

 much more power of de-amination than the other cells of the organism. The 

 experiments of Lang (1904) and of Miss Bostock (1911) have shown that tissues 

 in vitro are capable of de-aminating amino-acids to some extent, but that the 

 process is not quite the same as that in the living organism, since amides are more 

 readily acted on in vitro than are amino-acids, while the contrary is the case in the 

 organism. That the main part of the amino-acids absorbed by the intestine escape 

 immediate de-amination by the liver is also shown by the results of van Slyke and 

 Meyer (1912, p. 408). The blood of the femoral arteyy contained in one 

 experiment, before feeding, 3*7 mg. of amino-acid nitrogen per 100 c.c., and after 

 feeding, 8 '6 mg., while that of the portal vein, at the same time, contained very 

 little more, namely 9 -5 mg. This means that there was a loss of only 0'9 mg. in 

 traversing the liver, not more than would be expected if the liver only de-aminated 

 as much in proportion to its size as other organs. 



After large doses of amino-acids the de-aminated products can be detected in the urine. 

 Lactic acid from alanine (Neuberg and Langstein, 1903), glyceric acid from diamino-propionic 

 acid (Mayer, 1904) may be referred to. 



Moulds, bacteria, yeast, and the larvae of flies have also been shown to split 

 off ammonia from amino-acids. 



We may conclude that amino-acids are supplied to the tissues, and, with 

 the exception of that small part used for repair or growth, are de-aminated there. 



The fatty acid part is utilised for supply of energy and the next question 

 is the fate of the ammonia. 



The great activity of the liver in the conversion of ammonia to urea makes 

 it probable that the main part of the ammonia from the tissues is converted 

 into urea in this organ. When an Eck's fistula is made, that is, when a con- 

 nection is made between the portal vein and the vena cava, so that the liver 

 is practically cut out of the circulation, there is a great increase of ammonia 

 in the blood. Normally, also, there is much more ammonia in the portal blood 

 going to the liver than in that of the hepatic veins coming from it. The 

 investigations of Nencki and of Salaskin may be consulted (see Cathcart's 

 monograph, 1912, p. 51). 



On the other hand, Folin and Denis (1912) hold that the tissues themselves 

 have the power of converting ammonia into urea. They find that the urea 

 content of the blood of the hepatic vein, after the injection into the lumen of 

 the intestine of various proteins and amino-acids, is not greater than that of 



