Since glucose normalizes the impaired function of the citric acid cycle during ketogenesis, a study has been made of the effect of glucose on the inhibited cycle during ethanol metabolism in rat liver slice experiments. A calculation indicated that in the absence of glucose, the function of the cycle would have been totally blocked, to judge from the CO2 formation. The addition of glucose to the medium increased the CO2 production. Glucose up to an amount of 3 mM increased the rate of ethanol oxidation, but no further effect was observable with additional glucose. Only 6-8 per cent of the ethanol metabolized was broken down to CO2, and this amount was unaffected by glucose. No influence was exercised on the glycolytic end products lactate plus pyruvate, but the lactate/pyruvate ratio rose with an increase of glucose in the medium. As evidence exists that the impaired function of the citric acid cycle is attributable to the shift in the redox state of the liver which occurs during ethanol oxidation, and as glucose increases this shift, it can be assumed that glucose does not exercise any influence upon the function of the cycle during ethanol oxidation. The augmentation of CO2 formation with increasing amounts of glucose must be produced in decarboxylation reaction outside the citric acid cycle. © 1969.