Sparing of palmitic acid oxidation by carbohydrate: prefeeding versus addition to medium.

It is generally recognized that the pathways of fatty acid breakdown and of glucose catabolism (Embden-Meyerhof scheme) are confluent at the level of the 2-carbon fragment (acetyl-S-CoA). Nevertheless, several observations suggest an interplay between the metabolism of carbohydrate and that of fatty acids at a higher level: (a) Rats forcibly fed carbohydrate, as opposed to those fasted, exhibit a depressed capacity for oxidation of injected fatty acids. In the case of palmitic acid, this depressed oxidation was shown to represent principally a restriction in breakdown of the fatty acid molecule rather than a diversion of the 2-carbon breakdown product from an oxidative to a synthetic pathway (1). (b) Parenterally administered insulin, which promotes carbohydrate utilization, restricts the catabolism of palmitic acid by intact diabetic rats and by the isolated livers of the animals (2). (c) Glucose supplementation in vitro increases the direct esterification of octanoic and hexanoic acids by the rat mammary gland (3). Recently Allen et al. (4) failed to obtain a sparing of fatty acid oxidation when slices of liver, kidney, heart, and brain were incubated with C14-labeled palmitic acid in the presence of added glucose. They concluded that dietary carbohydrate does not lower fatty acid oxidation. Since we have drawn the opposite conclusion from experiments with intact animals, we have compared here the action of glucose fed to the rat before excision of its liver with the action of carbohydrate added directly to the incubation medium upon the oxidation of palmitic acid by liver slices.