TRIGLYCERIDES AND FATTY AOTDS 179 



ketone bodies present in the liver slices and substrate were reduced when 

 the samples were obtained from well-fed rats, as contrasted with samples 

 from fasted rats, but also that the consumption of butyrate from the 

 substrate in the former case was at a considerably higher level than that 

 in the liver slices from fasted rats. Thus, in the presence of carbohydrates, 

 livers utilized significantly greater amounts of ketogenic acids in the sub- 

 strate, and smaller quantities of ketone bodies remained unoxidized at the 

 end of the incubation than could be noted in experiments in which liver 

 slices were obtained from starved animals. Weinhouse et al}^^ also re- 

 ported that the presence of carbohydrate did not cause inhibition of the 

 oxidation of C2 to Cs fatty acids by liver slices, but that, in many cases, 

 it actually resulted in an increased rate of fatty acid oxidation. In the 

 absence of oxaloacetate, an accumulation of acetyl groups leads to their 

 self-condensation, with the formation of acetoacetate. These authors^^^ 

 suggest that this is the explanation for the findings of Bobbitt and DeueP^^ 

 that glycogen added to liver slices increased the rate of butyrate utilization 

 but decreased the rate of ketogenesis. 



Although Edson""^ postulates that carbohydrates and their derivatives 

 are antiketogenic and compete with carbohydrates for oxygen in the liver, 

 his results are inferential, since they are not based upon a direct determina- 

 tion of the decrease in fatty acids. However, the conclusions of Bobbitt 

 and DeueP^^ upon which they base their opinion that ketolysis best ex- 

 plains the action of carbohydrate on ketosis, are arrived at from experi- 

 ments involving the determination not only of the ketone bodies present 

 but also of the fatty acid disappearance during the course of an experiment. 



(c) Resume of the Mechanism of Action of Carbohydrate on Ketonuria. 

 The most logical concept of the action of carbohydrate in depressing ketosis 

 is that expressed by Rosenfeld^'^'* many years ago, and cited earlier, namely 

 that "fats burn in the flame of carbohydrate." Ketone bodies are broken 

 down to active acetate, and this combines with oxaloacetate, and so enters 

 the tricarboxylic cycle. When carbohydrate is present, so that the tri- 

 carboxylic acid cycle is functioning at a high level, adequate supplies of 

 oxaloacetate are available to bring about the removal of all the ketone 

 bodies formed. On the other hand, when the carbohydrate metabolism 

 is at a minimum level, and hence the supply of oxaloacetate arising from 

 carbohydrate is limited, there is insufficient oxaloacetate present to com- 

 bine with all the available active acetate. The reaction of ketone bodies 

 — »- active acetate becomes bogged down, and greater amounts of ketone 

 tjodies are retained in the tissues, in addition to those excreted. 



Thus, most evidence indicates that the action of carbohydrate in the 



