In livers from fed rats perfused with recirculating blood, infusion of ethanol produced an inhibition of ketogenesis followed by substantially increased production. Perfusate lactate concentrations fell markedly following the increase in ketone body formation. In these experiments perfusate acetate rose continuously, reaching a concentration of 10 mM at 70 min, while in a control liver concentrations remained very low. During non-recirculating perfusion with 3 mM acetate there was output of lactate, whereas at 10 mM acetate ketogenesis was greatly stimulated and there was net lactate uptake. These data support the concept that there is a concentration of acetate in the region of 5 mM, below which it competes with lactate for lipogenesis. Above this level acetate may penetrate the mitochondrion and stimulate ketogenesis and gluconeogenesis. Effects of ethanol in vitro may depend on the concentrations of acetate attained in the experimental system.

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http://dx.doi.org/10.1016/0304-4165(84)90099-0DOI Listing

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