Effect of Chronic Alcohol Consumption on Ethanol and Acetaldehyde Metabolism

  • C. S. Lieber
  • L. M. DeCarli
  • L. Feinman
  • Y. Hasumura
  • M. Korsten
  • S. Matsuzaki
  • R. Teschke
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 59)


Hepatic metabolism of ethanol to acetaldehyde by the alcohol dehydrogenase (ADH) pathway is associated with the generation of reducing equivalents as NADH. Conversely, reducing equivalents are consumed when ethanol oxidation is catalyzed by the NADPH dependent microsomal ethanol oxidizing system (MEOS). Since the major fraction of ethanol metabolism proceeds via ADH and since the oxidation of acetaldehyde also generates NADH, an excess of reducing equivalents is produced. This explains a variety of effects following acute ethanol administration, including hyperlactacidemia, hyper-uricemia, enhanced lipogenesis and depressed lipid oxidation. To the extent that ethanol is oxidized by the alternate MEOS pathway, it slows the metabolism of other microsomal substrates. Following chronic ethanol consumption, adaptive microsomal changes prevail, which include enhanced ethanol and drug metabolism, and increased lipoprotein production. Eventually, injury develops with alterations of the rough endoplasmic reticulum and structural and functional abnormalities of the mitochondria.

Ethanol exerts different effects on hepatic cellular metabolism, depending mainly on the duration of its intake. In the presence of ethanol following an acute load, a number of hepatic functions are inhibited including lipid oxidation and microsomal drug metabolism. In its early stages, chronic ethanol consumption produces adaptive metabolic changes in the endoplasmic reticulum which result in increased metabolism of ethanol and drugs and accelerated lipoprotein production. Prolongation of ethanol intake damages cell organelles and may result in hepatic lesions such as alcoholic hepatitis and cirrhosis. The purpose of this review is to describe some of the mechanisms involved in each of these stages and, when possible, to relate these changes to the metabolism of ethanol and acetaldehyde.


Ethanol Consumption Alcoholic Hepatitis Perfuse Liver Liver Slice Ethanol Oxidation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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© Springer Science+Business Media New York 1975

Authors and Affiliations

  • C. S. Lieber
    • 1
  • L. M. DeCarli
    • 1
  • L. Feinman
    • 1
  • Y. Hasumura
    • 1
  • M. Korsten
    • 1
  • S. Matsuzaki
    • 1
  • R. Teschke
    • 1
  1. 1.Section and Laboratory of Liver Disease and Nutrition Bronx Veterans Administration Hospital and Department of Medicine, Mount Sinai School of Medicine of the CityUniversity of New YorkNew YorkUSA

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