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In studying the effects of ethanol on the liver, we have directed our attention to the manner by which ethanol intoxication in animals causes an acute fatty liver (1, 2). Although the mechanism involved is still not well understood, the production of the fatty liver under these conditions probably involves one or more of the following four processes: 1) increased hepatic lipid synthesis, 2) decreased hepatic lipid utilization (e.g., oxidation), 3) increased transport of fatty acids from peripheral fat depots or 4) decreased release of lipid from the liver. Mallov and Bloch (1) originally suggested that the fatty liver following ethanol administration was due to an increased transport of fat from the depots to the liver, but later (3) considered that the increased hepatic lipid might be the result of increased hepatic fatty acid synthesis. Consistent with the latter concept are the observations of Lieber, DeCarli and Schmid (4, 5) that ethanol, in vivo and in vitro, stimulates fatty acid synthesis in the liver. These authors attributed the enhanced fatty acid synthesis to an increased production of reduced diphosphopyridine nucleotide (DPNH) produced by the oxidation of ethanol (5). On the other hand, good evidence has been presented recently (6, 7) that increased transport of fatty acids to the liver from the fat depots may be the major mechanism for the fatty liver produced by ethanol as well as by other agents, such as ethionine and carbon tetrachloride. To gain further insight into the mechanism whereby ethanol intoxication produces a fatty liver, we have investigated the four processes referred to above in order to determine the extent to which one or more of them may be involved.

STUDIES ON THE PATHOGENESIS OF THE ETHANOL-INDUCED FATTY LIVER. I. SYNTHESIS AND OXIDATION OF FATTY ACIDS BY THE LIVER*