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Abstract

Ethanol can be synthesized endogenously in trace amounts1 including bacterial fermentation in the gut2; it is however primarily an exogenous compound that is readily absorbed from the gastrointestinal tract. Only 2–10 % of that absorbed is eliminated through the kidneys and lungs; the rest must be oxidized in the body, principally in the liver. The rate of disappearance of ethanol from the blood is indeed remarkably decreased or halted by hepatectomy or procedures damaging the liver3. Moreover, the predominant role of the liver for ethanol metabolism was shown directly in individuals with portacaval shunts undergoing hepatic vein catheterization4. Extrahepatic metabolism of ethanol, although it occurs, is small5,6. This relative organ specificity of ethanol for the liver probably explains why, despite the existence of intracellular mechanisms responsible for redox homeostasis, ethanol oxidation produces striking metabolic imbalances in the liver. These effects are

Table 1.1 Characteristics of ethanol metabolism

aggravated by the lack of feedback mechanism to adjust the rate of ethanol oxidation to the metabolic state of the hepatocyte, and the inability of ethanol, unlike other major sources of calories, to be stored or metabolized to a marked degree in peripheral tissues (Table 1.1). The hepatocyte contains three main pathways for ethanol metabolism, each located in a different subcellular compartment: the alcohol dehydrogenase pathway of the cytosol or the soluble fraction of the cell, the microsomal ethanol oxidizing system located in the endoplasmic reticulum and catalase located in the peroxisomes.

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Lieber, C.S. (1977). Metabolism of Ethanol. In: Lieber, C.S. (eds) Metabolic Aspects of Alcoholism. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-6153-4_1

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