216 IV. CONVERSION OF FAT TO CARBOHYDRATE 



support the hypothesis that acetic acid is formed in the Hvers of normal or 

 diabetic animals, except those of Cook and Harrison. ^^ It is suggested by 

 the former workers that, in the diabetic animals, acetic acid can be assumed 

 to originate from the oxidizing agents used in the analyses. 



The bulk of the experimental evidence indicates that no increase in car- 

 bohydrate reserves results when acetate is given. However, Geelmuyden^" 

 reported that acetic acid is converted to glucose in the phlorhizinized dog 

 when fed along with a carbohydrate diet, but the evidence can hardly be 

 considered to be convincing. For example, the experiments are based upon 

 data in which the following D:N ratios^ were obtained: fourth day, 7.6; 

 fifth day, 6.8; sixth day (acetate administered), 6.6; and seventh day, 7.0. 

 During these days, the total glucose excretion was 57.0, 55.1, 58.0, and 

 65.3 g., respectively.^'*" In contradistinction to these results, both Ringer 

 and Lusk*' and Deuel and Milhorat''- failed to observe formation of sugar 

 when acetate was given to the phlorhizinized fasting dog. Geelmuyden'*" 

 suggested that acetic acid is not readily utilized, and that its conversion 

 to glucose may be delayed as much as twenty-four hours. It is 

 difficult to accept this hypothesis for a substance as readily metabolized as 

 acetate. Moreover, it is without precedent in a wide range of carbohydrate 

 intermediates and amino acids which have been investigated by the glyco- 

 gen and phlorhizin technic. 



Negative results have been noted by other workers, as regards the ability 

 of acetate to give rise to glycogen. Thus, Ponsford and Smedley-Mac- 

 Lean,*^ and also Majer and Reisner,'** found no glycogen formation in rats 

 following the administration of fats containing acetic acid. Similar data 

 were recorded by Stohr^^ for fasting rats, although slightly higher than con- 

 trol values were noted when acetate was fed concomitantly with large doses 

 of glucose. Clutterbuck'*^ also observed that the addition of acetate to 

 minced tissues of rabbits did not result in the formation of succinic acid, 

 which might be an intermediate stage in glucose formation. On the other 

 hand, Thunberg*^ found that succinic acid may originate from acetic acid 

 in the animal organism. Since the former compound is undoubtedly a 



33 R. P. Cook and K. Harrison, Biochem. J., 30, 1640-1643 (1936). 

 « H. C. Geelmuvden, Skand. Arch. Physiol, 40, 211-225 (1920). 

 *^ A. I. Ringer and G. Lusk, Z. physiol. Chem., 66, 106^119 (1910). 

 « H. J. Deuel, Jr., and A. T. Milhorat, /. Biol. Chem., 78, 299-309 (1928). 

 " A. P. Ponsford and I. Smedley-MacLean, Biochem. J., 26, 1340-1344 (1932). 

 ^« E. H. Majer and H. Reisner, Biochem. Z., 263, 340-352 (1933). 

 «R. Stohr, Z. physiol. Chem., 217, 141-152 (1933); 220, 27-33 (1933). 

 ^8 P. W. Clutterbuck, Biochem. J., 21, 512-521 (1927). 



« T. Thunberg, Skarid. Arch. Physiol, 25, 37-84 (1911); 35, 163-195 (1918); Physiol. 

 AbsL, 2, 665 (1918). 



