43 8 METABOLISM, NUTRITION AND DIET 



alone given, there was a loss of 118 grams. In these cases gelatin did not 

 take the place of protein in any sense, but rather saved it from oxidation as 

 a source of energy. The protein was so protected that, instead of being used 

 up, it helped to form tissue and increased the body weight. Gelatin, there- 

 fore, saved the protein material for constructive processes. 



Murlin has investigated more exactly the substitution of gelatin for the 

 mixed proteins in the food. In a series of experiments on dogs, the nitrogen 

 output was first determined during fasting periods. Varying amounts 

 of gelatin containing from a fourth to two-thirds of this amount of nitrogen 

 were then fed, the remaining three-fourths to one-third of the fasting quantity 

 being supplied in meat or other proteins. The calorific requirement of 

 the animal was made up in each experiment with fats and carbohydrates. 

 Results show an equal sparing of body protein, whether one-fourth, one- 

 third, or one-half of the fasting nitrogen was fed in the form of gelatin, 

 the coincident sparing of protein by fats and carbohydrates being the same. 

 When the coincident sparing of protein by non-nitrogenous food was in- 

 creased by feeding a larger percentage of carbohydrates and less fat, the 

 fraction of the fasting nitrogen fed in the form of gelatin could be raised to 

 two-thirds, the other one-third being fed in meat. Nitrogenous equilibrium 

 was maintained on this diet for several days. The same result was obtained 

 on man. The evidence at hand indicates that other individual proteins, 

 in which certain amino acid constituents are deficient in quantity or which 

 are absent, like gelatin would not replace entirely the ordinary mixed 

 protein requirements. 



The Formation of Urea. The nitrogenous fraction of the protein mole- 

 cule is in the end converted largely into urea and is excreted from the body in 

 that form, as described in the chapter on Excretion. The method of forma- 

 tion of urea as well as the place where this occurs has given rise to great 

 controversy, while the intermediate products between proteins and urea 

 have not as yet been fully determined. We can state with certainty that 

 urea is not formed in the kidneys, since it is not only found in the blood of 

 the renal artery, but it accumulates in the blood if the kidneys are diseased 

 or removed and the separation of the urine is interfered with. Circulation 

 of blood through the kidney does not result in the formation of more urea 

 than is present in the blood to begin with. 



There are a number of experiments that prove that urea is formed in the 

 liver. The power of the liver cells to form urea is shown by the increase of 

 urea in the blood leaving an isolated living liver through which an artificial 

 circulation is kept up. When ammonium carbamate and other ammonium 

 salts are added to the blood, the urea increases more rapidly and to a greater 

 extent. This change occurs even when the living hepatic tissue is chopped 

 up and simply mixed with the ammonium compounds in a beaker. 



If blood from a well-fed animal be circulated through the isolated liver, 



