Abstract
It is well known that the most common manifestation of alcohol hepatotoxicty is the occurrence of a fatty liver, that is to say, an increase in the hepatic triacylglycerol level. Such an increase can be reproduced experimentally even by a single ethanol administration. It is still subject to debate whether the fatty liver induced by such administration is due to ethanol metabolism, resulting in an enhanced production of reducing equivalents in the hepatocyte and thereby inhibiting fatty acid oxidation. However other experimental data, such as those of Kalant, Khanna, Seymour, and Loth (1975), have brought arguments in favor of the role of ethanol per se, acting through an unspecific stress action, independent from ethanol metabolism.
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Nordmann, R., Beaugé, F., Clément, M., Nordmann, J. (1989). Metabolism Through Alcohol Dehydrogenase is Not a Prerequisite for Fatty Liver Induction by Alcohols. In: Einstein, S. (eds) Drug and Alcohol Use. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0888-9_32
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DOI: https://doi.org/10.1007/978-1-4899-0888-9_32
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