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To study if the acute ethanol-induced increase in the liver triglyceride concentrations in fasted rats is influenced by the blood ethanol concentration when the ethanol oxidation proceeds at a maximal rate, rats fasted for 24 h were given ethanol by continuous i.v. infusion to maintain the blood ethanol concentrations at about 10 or 45 mmol/l. Control rats were given saline. The calculated rate of ethanol oxidation was similar in the two ethanol-treated groups. The incorporation of radioactivity from [9,10-3H]oleic acid, injected through an arterial cannula in the aorta, into the liver triglycerides was increased over control values to the same extent in the two ethanol-treated groups. Thus, the ethanol oxidation proceeded at a similar high rate, and a similar increase in the utilization of plasma free fatty acids for synthesis of liver triglycerides, previously proposed as a major mechanism for the development of the acute ethanol-induced fatty liver, occurred at both blood ethanol concentrations. The liver triglyceride concentrations, on the other hand, were increased over control values in rats with about 45 mmol/l ethanol in the blood but not in rats with about 10 mmol/l ethanol in the blood. At least in part this could be attributed to a decrease in the plasma free fatty acid concentration at the low blood ethanol concentration.
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O. Johnson (1974) studied this question.
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