200 III. OXIDATION AND METABOLISM 



rather than static. There can be no doubt that, m spite of the continuous 

 turnover of fats during periods of normal nutrition, there are certain condi- 

 tions under which fat oxidation is depressed, and other situations when fat 

 oxidation is accelerated. 



Geyer and associates'^ ^ demonstrated that the rate of palmitic acid oxida- 

 tion in liver shces, but not in kidney slices, of rats was accelerated by pre- 

 vious fasting. The addition of pyruvate to the medium decreased the rate 

 of oxidation of palmitic acid by liver and kidney slices from both non- 

 fasted and fasted rats. On the other hand, just the opposite condition to 

 that reported in fasting has been shown to obtain in congenitally obese 

 mice.'^^^ Thus, Salcedo and Stetten"- reported that the excess fat deposi- 

 tion in the congenitally obese strain maintained at Cold Spring Harbor re- 

 sulted from the retarded metabolism of the depot fatty acids, while the 

 proportion of dietary fatty acids directly stored was normal. In the tests 

 of Guggenheim and Mayer,'' ^^ it was found that, when fasted obese and non- 

 obese mice were injected with carboxyl-labeled sodium acetate, the non- 

 obese mice excreted one-third more labeled CO2 during the three hours 

 following the injection than did the obese animals. After labeled acetate 

 was fed for three days to these two groups of mice, the retention of isotopic 

 carbon was more than twice as great in the strain of congenitally obese 

 mice as m the normal animals. It is suggested that a partial block in ace- 

 tate utilization obtains, with a resultant increased hpogenesis. Pyruvate 

 oxidation is likewise depressed in the obese strain of mice. 



The results of Munoz and Leloir^^ were interpreted as indicative of varia- 

 tions in fat oxidation as related to the length of the fatty acid chains. 

 Thus, it was reported that fatty acids up to eight carbons in length caused 

 a rapid mcrease in O2 uptake of a homogenate of guinea pig liver, while 

 fatty acids of twelve to eighteen carbons either caused no augmentation of 

 oxygen uptake or resulted in an inhibition of this utilization. Weinhouse 

 et al.^^^ have also shown that, whereas palmitic acid is converted both to 

 CO2 and to acetoacetate by rat liver slices and homogenates, the lower 

 fatty acids are transformed chiefly to ketone bodies. However, Weinhouse 

 and co-workers^*® conclude that the same enzyme systems are involved in 

 the oxidation of both longer- and shorter-chain acids. 



Various parts of the fatty acid molecule appear to be oxidized simul- 

 taneously. Weinman et alJ^'^ found that rats injected with tripalmitin in 



'" R. P. Geyer, E. J. Bowie, and J. C. Bates, /. Biol. Chem., 200, 271-274 (1953). 

 "2 J. Salcedo, Jr., and De W. Stetten, Jr., /. Biol. Chem., 151, 413-416 (1943). 

 '13 K. Guggenheim and J. Mayer, /. Biol. Chem., 198, 259-265 (1952). 

 '1^ E. O. Weinman, I. L. Chaikoff, W. G. Dauben, M. Gee, and C. Entenman, /. Biol. 

 Chem., 184, 735-744 (1950). 



