TRIGLYCERIDES AND FATTY ACIDS 163 



production of acetoacetate in rats treated with anterior pituitary hormone, 

 which resulted in a ketonemia. It is suggested by the latter workers 

 that this may result from an increased ketone body formation in the liver 

 due to a decrease in carbohydrate metabolism. Kinsell d al^°^ noted that 

 testosterone propionate exerted a beneficnal effect on the ketonuria in a 

 diabetic patient. It is suggested that this may have been due in part to a 

 direct effect of testosterone upon fat or ketone metal)olism. 



e. The Mechanism of the Effect of Carbohydrate on Ketonuria. It has 

 long been recognized that a close relationship obtains between the ap- 

 pearance of ketone bodies in the blood or urine and the failure to oxidize 

 carbohydrate. One of the most familiar aphorisms is the statement of 

 Rosenfeld^^^ that "fats burn in the flame of carbohydrates." This was 

 modernized by Woodyatt^^" in 1916 to the following statement: "When 

 the mixture of metabolites oxidizing in the body contains more than three 

 molecules of higher fatty acid to one of glucose, then the body 'smokes' 

 with acidosis compounds like an automobile with too much oil in the 

 cylinders." The subject of the interrelationship of ketosis and carbo- 

 hydrate oxidation has been reviewed by Deuel and Morehouse,^" and also 

 by Stadie.^ 



As early as 1895, Hirschfeld"'' recognized that the condition responsible 

 for ketone body production is a failure in carbohydrate metabolism. 

 A similar concept of the concurrent oxidation of carbohydrate and fat was 

 held by Geelmuyden,^i"'^i^ g^j^(j j^ ^ag ^^g basis for the theory of Shaffer-" 

 that a quantitative ratio must exist between the antiketogenic and the 

 ketogenic fractions if ketonuria is to be prevented. The original concept 

 of Shaffer^^^ was based upon in vitro experiments in which it was demon- 

 strated that the presence of glucose was essential if acetoacetate was to 

 be destroyed in alkaline solution with H2O2. Ultimately, Shaffer^^ 

 suggested that two molecules of acetoacetate were destroyed for each 

 molecule of glucose oxidized. It was suggested and demonstrated 

 from calculations of published experiments that any excess acetoacetate 

 over that accounted for on a ketogenic : antiketogenic ratio of 2:1 was 

 excreted. ^^^'"^ On the other hand, Woodyatt^''^ suggested that 1 g. of 



W9 L. W. Kinsell, S. Margen, G. D. Michaels, and D. P. McCallie, /. Clin. Invest., SO, 

 1486-1490 (1951). 



610 R. T. Woodyatt, /. Am. Med. A.ssoc., 66, 1910-1913 (1916). 



6" H. J. Deuel, Jr., and M. G. Morehouse, Advances in Carbohydrate Cheni., 2, 119-160 

 (1946). 



6'2H. C. Geelmuyden, Z. physiol. Chem., 4I, 128-152 (1904). 



613 H. C. Geelmuyden, Z. physiol. Chem., 58, 255-271 (1908-1909). 



""P. A. Shaffer, J. Biol. Chem., 47, 433-448 (1921). 



