Abstract
It has been demonstrated that a single oral dose of ethanol will elevate the triglyceride content in rat liver (1). However, there is no agreement on the mechanism of this effect. Lieber and Schmid have presented data which suggests that ethanol increases the incorporation of C-14 labelled acetate in vivo or in vitro into long chain fatty acids of rat liver (2,3). These workers have proposed that the increased NADH which is generated by ethanol oxidation stimulates fatty acid synthesis. Data by other workers, however, have not confirmed these results (4,5,6). In addition, Bortz et al (7) have shown that the rate of incorporation of acetate into long chain fatty acids in the liver is controlled by the acetyl-CoA-carboxylase catalyzed reaction: ▪ This reaction precedes the reductive steps in the fatty acid synthetase system (reaction 2), during which the reduced pyridine nucleotides produced by ethanol oxidation would be used. ▪ Reaction 1 can be selectively inhibited by feeding animals a fatty meal or by starvation (7,8). Under these conditions it should be possible to test whether ethanol can drive the over-all rate of lipogenesis by a mass action effect on reaction 2. In addition some information on the influence of ethanol on reaction 1 under these conditions may be obtained. Accordingly, we have investigated the effect of ethanol on lipogenesis in the livers of animals which have been either fed a fatty meal or have been fasted.
Published Version
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