Molecular and cellular events in alcohol-induced muscle disease

Joaquim Fernandez-Solà, Victor R. Preedy, Charles H. Lang, Emilio Gonzalez-Reimers, M. Arno, J. C I Lin, H. Wiseman, S. Zhou, P. W. Emery, T. Nakahara, K. Hashimoto, M. Hirano, F. Santolaria-Fernández, T. González-Hernández, Francesc Fatjó, Emilio Sacanella, Ramón Estruch, José M. Nicolás, Alvaro Urbano-Márquez

Research output: Contribution to journalReview article

50 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1953-1962
Number of pages10
JournalAlcoholism: Clinical and Experimental Research
Volume31
Issue number12
DOIs
StatePublished - Dec 1 2007

Fingerprint

Muscular Diseases
Muscle
Alcohols
Muscles
Skeletal Muscle
Ethanol
Apoptosis
Gene Expression
Alcoholic Intoxication
Proteins
Muscular Atrophy
Gene expression
Trace Elements
Muscle Strength
Proteome
Research
Alcohol Drinking
Muscle Cells
Lipid Peroxidation
Oxidative Stress

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Toxicology
  • Psychiatry and Mental health

Cite this

Fernandez-Solà, J., Preedy, V. R., Lang, C. H., Gonzalez-Reimers, E., Arno, M., Lin, J. C. I., ... Urbano-Márquez, A. (2007). Molecular and cellular events in alcohol-induced muscle disease. Alcoholism: Clinical and Experimental Research, 31(12), 1953-1962. https://doi.org/10.1111/j.1530-0277.2007.00530.x
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. / Molecular and cellular events in alcohol-induced muscle disease. In: Alcoholism: Clinical and Experimental Research. 2007 ; Vol. 31, No. 12. pp. 1953-1962.
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abstract = "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.",
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Fernandez-Solà, J, Preedy, VR, Lang, CH, Gonzalez-Reimers, E, Arno, M, Lin, JCI, Wiseman, H, Zhou, S, Emery, PW, Nakahara, T, Hashimoto, K, Hirano, M, Santolaria-Fernández, F, González-Hernández, T, Fatjó, F, Sacanella, E, Estruch, R, Nicolás, JM & Urbano-Márquez, A 2007, 'Molecular and cellular events in alcohol-induced muscle disease', Alcoholism: Clinical and Experimental Research, vol. 31, no. 12, pp. 1953-1962. https://doi.org/10.1111/j.1530-0277.2007.00530.x

Molecular and cellular events in alcohol-induced muscle disease. / 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.

In: Alcoholism: Clinical and Experimental Research, Vol. 31, No. 12, 01.12.2007, p. 1953-1962.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Molecular and cellular events in alcohol-induced muscle disease

AU - Fernandez-Solà, Joaquim

AU - Preedy, Victor R.

AU - Lang, Charles H.

AU - Gonzalez-Reimers, Emilio

AU - Arno, M.

AU - Lin, J. C I

AU - Wiseman, H.

AU - Zhou, S.

AU - Emery, P. W.

AU - Nakahara, T.

AU - Hashimoto, K.

AU - Hirano, M.

AU - Santolaria-Fernández, F.

AU - González-Hernández, T.

AU - Fatjó, Francesc

AU - Sacanella, Emilio

AU - Estruch, Ramón

AU - Nicolás, José M.

AU - Urbano-Márquez, Alvaro

PY - 2007/12/1

Y1 - 2007/12/1

N2 - 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.

AB - 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.

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U2 - 10.1111/j.1530-0277.2007.00530.x

DO - 10.1111/j.1530-0277.2007.00530.x

M3 - Review article

VL - 31

SP - 1953

EP - 1962

JO - Alcoholism: Clinical and Experimental Research

JF - Alcoholism: Clinical and Experimental Research

SN - 0145-6008

IS - 12

ER -