Alcoholic myopathy and acetaldehyde

Victor R. Preedy, David W. Crabb, Jaume Farrés, Peter W. Emery

Research output: Chapter in Book/Report/Conference proceedingConference contribution

15 Scopus citations


Alcoholic myopathy is characterized by biochemical and morphological lesions within muscle, ranging from impairment of muscle strength and loss of lean tissue to cellular disturbances and altered gene expression. The chronic form of the disease is five times more common than cirrhosis and is characterized by selective atrophy of type II (anaerobic) fibres: type I (aerobic) fibres are relatively protected. Although the causative agent is known (i.e. ethanol), the intervening steps between alcohol ingestion and the development of symptoms and lesions are poorly understood. However, acetaldehyde appears to have an important role in the aetiology of the disease. For example, alcohol is a potent perturbant of muscle protein synthesis in vivo, and this effect is exacerbated by cyanamide pre-dosage, which raises acetaldehyde concentrations. Acetaldehyde alone also reduces muscle protein synthesis in vivo and proteolytic activity in vitro. The formation of acetaldehyde protein adducts is another mechanism of putative importance in alcoholic myopathy. These adducts are formed within muscle in response to either acute or chronic alcohol exposure and the adducts are located preferentially within the sarcolemmal and sub-sarcolemmal regions. However, the significance of protein adduct formation is unclear since we do not currently know the identity of the adducted muscle proteins nor whether adduction alters the biochemical or functional properties of skeletal muscle proteins.

Original languageEnglish (US)
Title of host publicationAcetaldehyde-Related Pathology
Subtitle of host publicationBridging the Trans-Disciplinary Divide
Number of pages20
StatePublished - Dec 1 2007

Publication series

NameNovartis Foundation Symposium
ISSN (Print)1528-2511

ASJC Scopus subject areas

  • Medicine(all)

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