Molecular and Cellular Events in Alcohol-Induced Muscle Disease

Alcohol consumption induces a dose‐dependent noxious effect on skeletal muscle, leading to progressive functional and structural damage of myocytes, with concomitant reductions in lean body mass. Nearly half of high‐dose chronic alcohol consumers develop alcoholic skeletal myopathy. The pathogenic m...

Full description

Saved in:
Bibliographic Details
Published inAlcoholism, clinical and experimental research Vol. 31; no. 12; pp. 1953 - 1962
Main Authors Fernandez-Solà, Joaquim, Preedy, Victor R., Lang, Charles H., Gonzalez-Reimers, Emilio, Arno, M., Lin, J. C. I., Wiseman, H., Zhou, S., Emery, P. W., Nakahara, T., Hashimoto, K., Hirano, M., Santolaria-Fernández, F., González-Hernández, T., Fatjó, Francesc, Sacanella, Emilio, Estruch, Ramón, Nicolás, José M., Urbano-Márquez, Alvaro
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.12.2007
Lippincott Williams & Wilkins
Subjects
Online AccessGet full text
ISSN0145-6008
1530-0277
1530-0277
DOI10.1111/j.1530-0277.2007.00530.x

Cover

More Information
Summary:Alcohol consumption induces a dose‐dependent noxious effect on skeletal muscle, leading to progressive functional and structural damage of myocytes, with concomitant reductions in lean body mass. Nearly half of high‐dose chronic alcohol consumers develop alcoholic skeletal myopathy. The pathogenic mechanisms that lie between alcohol intake and loss of muscle tissue involve multiple pathways, making the elucidation of the disease somewhat difficult. This review discusses the recent advances in basic and clinical research on the molecular and cellular events involved in the development of alcohol‐induced muscle disease. The main areas of recent research interest on this field are as follows: (i) molecular mechanisms in alcohol exposed muscle in the rat model; (ii) gene expression changes in alcohol exposed muscle; (iii) the role of trace elements and oxidative stress in alcoholic myopathy; and (iv) the role of apoptosis and preapoptotic pathways in alcoholic myopathy. These aforementioned areas are crucial in understanding the pathogenesis of this disease. For example, there is overwhelming evidence that both chronic alcohol ingestion and acute alcohol intoxication impair the rate of protein synthesis of myofibrillar proteins, in particular, under both postabsorptive and postprandial conditions. Perturbations in gene expression are contributory factors to the development of alcoholic myopathy, as ethanol‐induced alterations are detected in over 400 genes and the protein profile (i.e., the proteome) of muscle is also affected.There is supportive evidence that oxidative damage is involved in the pathogenesis of alcoholic myopathy. Increased lipid peroxidation is related to muscle fibre atrophy, and reduced serum levels of some antioxidants may be related to loss of muscle mass and muscle strength. Finally, ethanol induces skeletal muscle apoptosis and increases both pro‐ and antiapoptotic regulatory mechanisms.
Bibliography:ark:/67375/WNG-G7W853V0-Q
istex:F6C6BBA25589872377887AC6F445CA608F7C4F2C
ArticleID:ACER530
The subject of this review has been presented at the International Society Research on Alcoholism 2006 World Congress on Alcohol Research, September 10‐13, 2006, Sydney, Australia. Abstracts are included in Alcohol Clin Exp Res 2006; 30(Suppl):9.
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:0145-6008
1530-0277
1530-0277
DOI:10.1111/j.1530-0277.2007.00530.x