Exercise and skeletal muscle glucose transporter 4 expression: molecular mechanisms

McGee, Sean L. and Hargreaves, Mark 2006, Exercise and skeletal muscle glucose transporter 4 expression: molecular mechanisms, Clinical and experimental pharmacology and physiology, vol. 33, no. 4, pp. 395-399, doi: 10.1111/j.1440-1681.2006.04362.x.

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Title Exercise and skeletal muscle glucose transporter 4 expression: molecular mechanisms
Author(s) McGee, Sean L.ORCID iD for McGee, Sean L. orcid.org/0000-0001-6953-106X
Hargreaves, Mark
Journal name Clinical and experimental pharmacology and physiology
Volume number 33
Issue number 4
Start page 395
End page 399
Publisher Wiley-Blackwell Publishing Asia
Place of publication Richmond, Vic.
Publication date 2006-04
ISSN 0305-1870
Summary 1.      Skeletal muscle is a highly plastic tissue that has a remarkable ability to adapt to external demands, such as exercise. Many of these adaptations can be explained by changes in skeletal muscle gene expression. A single bout of exercise is sufficient to induce the expression of some metabolic genes. We have focused our attention on the regulation of glucose transporter isoform 4 (GLUT-4) expression in human skeletal muscle.

2.      Glucose transporter isoform 4 gene expression is increased immediately following a single bout of exercise, and the GLUT-4 enhancer factor (GEF) and myocyte enhancer factor 2 (MEF2) transcription factors are required for this response. Glucose transporter isoform enhancer factor and MEF2 DNA binding activities are increased following exercise, and the molecular mechanisms regulating MEF2 in exercising human skeletal muscle have also been examined.

3.      These studies find possible roles for histone deacetylase 5 (HDAC5), adenosine monophosphate–activated protein kinase (AMPK), peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) and p38 mitogen-activated protein kinase (MAPK) in regulating MEF2 through a series of complex interactions potentially involving MEF2 repression, coactivation and phosphorylation.

4.      Given that MEF2 is a transcription factor required for many exercise responsive genes, it is possible that these mechanisms are responsible for regulating the expression of a variety of metabolic genes during exercise. These mechanisms could also provide targets for the treatment and management of metabolic disease states, such as obesity and type 2 diabetes, which are characterized by mitochondrial dysfunction and insulin resistance in skeletal muscle.
Language eng
DOI 10.1111/j.1440-1681.2006.04362.x
Field of Research 060114 Systems Biology
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Persistent URL http://hdl.handle.net/10536/DRO/DU:30025015

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
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Created: Fri, 12 Mar 2010, 10:42:56 EST by Sean McGee

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