TRIGLYCERIDES AND FATTY ACIDS 197 



chief site of ketogenesis due to fatty acid dogiadatiou and by condensation 

 of acetic acid, muscle and other non-hepati(; tissues can form ketone bodies. 

 Thus, Medes and her co-workers,*'^^ employing isotopic acetate, reported 

 that ketogenesis is not exclusively a function of the liver, but that it may 

 take place in tissues, such as the kidney, which utilize acetate. 



Pennington^^^ reported that the epithelium of the reticulum and of the 

 omasum of the sheep were as active in transforming acetic and butyric 

 acids to ketone bodies as was liver tissue. However, the epithelia of the 

 abomasum, cecum, and kidney produced a relatively small amount of 

 ketone bodies. 



The epithelial tissue of sheep rumen is able to convert butyric acid in 

 vitro to ketone bodies.^^^'"*^^ Ketone bodies were also shown to originate 

 from acetic acid, but not from propionic acid; moreover, the latter com- 

 pound was found to exert an antiketogenic effect. ^^^ In a later study of the 

 reactions in the epithelial tissue of sheep rumen,'^'"' ketone bodies were pro- 

 duced quantitatively after the first 1.5 hours, from pyruvate, instead of the 

 latter compound being converted to lactate. Ketone bodies were also 

 produced from lactate, but at a slower rate than from pyruvate. In 

 coiitrast to these results, glucose was metabolized without the production 

 of ketone bodies, by the sheep rumen epithelia. Actually, glucose in the 

 presence of CO2 suppressed the endogenous production of ketone bodies, 

 although it did not decrease the amount of pyruvate metabolized. It is 

 suggested that, under these conditions, glucose is metabolized by a pathway 

 other than via pyruvic acid.^°° 



Isolated tissues other than the liver and, to some extent, the kidney, do 

 not yield ketone bodies^^^'^^^'^"^ m appreciable amounts. The relatively 

 slight degree of ketosis produced by kidney slices is attributed to the 

 rapid oxidation of acetoacetate by this tissue.^^* 



Greenbaum and McLean^"^ have suggested, on the basis of tests on rats, 

 that the growth hormone of the anterior lobe of the pituitary gland controls 

 the extrahepatic utilization of fat. Since the liver is unable to catabolize 

 the total fat disappearing from the body, it was concluded that the addi- 

 tional fat oxidized was cataboUzed outside of the liver, the growth hor- 

 mone being the stimulating agent. A definite ketonuria was shown to 

 obtam in adult female rats as a result of this catabolism. 



69' G. Medes, S. Weinhouse, and N. F. Flovd, /. Biol. Chem., 157, 751-752 (1945). 



"8 R. J. Pennington, Biochem. J., 51, 251-258 (1952). 



"9 R. J. Pennington, Biochem. J., 49, lix (1951). 



™o R. J. Pennington and T. M. Sutherland, Biochem. J., 54, xxvii (1953). 



™i R. A. Shipley, Am. J. Physiol, I4I, 662-6G8 (1944). 



™2 A. L. Greenbaum and P. McLean, Biochem-. J., 54, 413-424 (1953). 



