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    Histone deacetylase 5 regulates glucose uptake and insulin action in muscle cells

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    Author
    Raichur, S; Teh, SH; Ohwaki, K; Gaur, V; Long, YC; Hargreaves, M; McGee, SL; Kusunoki, J
    Date
    2012-12-01
    Source Title
    JOURNAL OF MOLECULAR ENDOCRINOLOGY
    Publisher
    BIOSCIENTIFICA LTD
    University of Melbourne Author/s
    Hargreaves, Ian
    Affiliation
    Physiology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Raichur, S., Teh, S. H., Ohwaki, K., Gaur, V., Long, Y. C., Hargreaves, M., McGee, S. L. & Kusunoki, J. (2012). Histone deacetylase 5 regulates glucose uptake and insulin action in muscle cells. JOURNAL OF MOLECULAR ENDOCRINOLOGY, 49 (3), pp.203-211. https://doi.org/10.1530/JME-12-0095.
    Access Status
    This item is currently not available from this repository
    URI
    http://hdl.handle.net/11343/32829
    DOI
    10.1530/JME-12-0095
    Description

    C1 - Journal Articles Refereed

    Abstract
    The class IIa histone deacetylases (HDACs) act as transcriptional repressors by altering chromatin structure through histone deacetylation. This family of enzymes regulates muscle development and phenotype, through regulation of muscle-specific genes including myogenin and MyoD (MYOD1). More recently, class IIa HDACs have been implicated in regulation of genes involved in glucose metabolism. However, the effects of HDAC5 on glucose metabolism and insulin action have not been directly assessed. Knockdown of HDAC5 in human primary muscle cells increased glucose uptake and was associated with increased GLUT4 (SLC2A4) expression and promoter activity but was associated with reduced GLUT1 (SLC2A1) expression. There was no change in PGC-1α (PPARGC1A) expression. The effects of HDAC5 knockdown on glucose metabolism were not due to alterations in the initiation of differentiation, as knockdown of HDAC5 after the onset of differentiation also resulted in increased glucose uptake and insulin-stimulated glycogen synthesis. These data show that inhibition of HDAC5 enhances metabolism and insulin action in muscle cells. As these processes in muscle are dysregulated in metabolic disease, HDAC inhibition could be an effective therapeutic strategy to improve muscle metabolism in these diseases. Therefore, we also examined the effects of the pan HDAC inhibitor, Scriptaid, on muscle cell metabolism. In myotubes, Scriptaid increased histone 3 acetylation, GLUT4 expression, glucose uptake and both oxidative and non-oxidative metabolic flux. Together, these data suggest that HDAC5 regulates muscle glucose metabolism and insulin action and that HDAC inhibitors can be used to modulate these parameters in muscle cells.
    Keywords
    Cell Metabolism; Diabetes

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