PATHOLOGICAL METABOLISM OF DIABETES 279 



to the quantity of fat actually catabolized. Of course especially in the 

 young lower ratios will also be seen. 



These figures apply in the case of the body taken as a whole. The 

 formation of acetone bodies is a process which appears to be confined very 

 largely to the liver. Recently Witzemann has discussed the peculiar pro- 

 clivity of the liver to form acetone from butyric acid in relationship with 

 the ammonia metabolism of the liver. Ammonia was the base that Dakin 

 used in his oxidation of butyric acid with hydrogen peroxid when he first 

 demonstrated the possibility of producing acetone bodies from the oxida- 

 tion of fatty acids in the test tube. Witzemann shows that the power of 

 ammonium to induce acetone formation is not shared in equal degree by 

 alkalis in general, but is a specific property of ammonia itself, and that 

 even the sodium and potassium salts of butyric acid when oxidized in the 

 presence of ammonia, yield more acetone than in the absence of ammonia. 

 Possibly that interaction between oxidizing glucose and oxidizing fatty 

 acids that destroys acetoacetic acid or prevents its accumulation in abnor- 

 mal quantities ("ketolysis," "antiketogenesis") also occurs chiefly in the 

 liver, in which case the ratio above discussed may be particularly affected 

 by variations in the size or condition of the liver. Migrainics, epileptics 

 and others with disordered hepatic functions would not be expected to 

 behave in this respect exactly as normals. 



For clinical pan-poses, it may be calculated that 100 grams of mixed 

 fat in the diet, if completely absorbed and catabolized, will introduce 

 into the metabolism about 90 grams of higher fatty acid. Protein of the 

 diet, or tissues, is resolved into amino-acids and in so far as these are ab- 

 sorbed and catabolized, they must be deaminized (and presumably at the 

 same time oxidized) to yield oxy or hydroxy acids. Of these a part is 

 convertible into glucose, another part into P-hydroxybutyric and aceto- 

 acetic acids, while a third small fraction is destroyed in as yet unknown 

 ways. 100 grams of protein introduce a certain quantity of products 

 which are the equivalent of products of the higher fatty acid catabolism 

 in that they are capable of yielding (3-hydroxy and acetoacetic acids. The 

 exact quantity of these substances formed in the catabolism of 100 grams of 

 protein can be only roughly estimated. The amino-acids that are certainly 

 known to yield acetone bodies are leucin, tyrosin and phenyl alanin. If 

 we take the quantities of these amino acids found in 100 gm. of ox muscle 

 protein by Osborne and Mendel, as Shaffer has also done and convert the 

 weights given into gram molecules, we obtain 0.16 gram molecules of these 

 ketogenic amino acids (per 100 gm. protein). If we assume that each of 

 these molecules of amino-acid is capable of yielding 1 molecule of aceto- 

 acetic (or (3-hydroxybutyric acid) and accept the view that 1 molecule of a 

 higher fatty acid such as oleic or palmitic acid also yields 1 molecule 

 of acetoacetic (or (5-hydroxybutyric) acid in the course of its catabolism, 

 then the 0.16 gram molecule of ketogenic amino-acids would be equivalent 



