Abstract
The rate of incorporation of labeled acetate into cholesterol by liver slices of pyridoxine-deficient rats was found to be three times that of control rats; with liver homogenates the difference between the two groups was even greater. Using the CO2 trapping technique, a 30% decrease in the hepatic acetate pool size was observed in pyridoxine-deficient rats and a 20% increase in pair-fed rats. Activity of the Krebs cycle was decreased by a third in the pair-fed rats.
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