Effects of Pyruvate and Krebs' Cycle Intermediates on Hepatic Acetate Metabolism in Relation to Cold Exposure and Fasting

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Abstract
Liver slices were prepared from ‘control’ rats kept at 25°C, from fed and fasted rats kept at 0–2°C for 1 day, and from rats kept at 25°C without food for 1 day. The slices were incubated with sodium acetate-C14 at 37.5°C. The incorporation of the acetate-C14 into CO2, fatty acids and cholesterol was measured. The depressed acetate oxidation found in liver slices from ‘cold-fasted’ rats was reversed by the addition of glucose, pyruvate, or succinate to the incubation medium, the first two with equal effectiveness, the succinate less so. The fact that a certain minimum level of carbohydrate metabolism is needed to support hepatic acetate oxidation appears to be a function of the extent of pyruvate metabolism. Pyruvate stimulates hepatic lipogenesis from acetate to a much less extent than does glucose, while succinate has no effect at all on this process. The data indicate that the effect of carbohydrate metabolism on acetate lipogenesis is a function of processes occurring before the formation of pyruvate. Cholesterogenesis was for the most part unaffected by the substrates studied, and when an effect occurred, it could very well have been a function of isotope dilution.

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