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

Raichur, Suryaprakash, Hooi-Teh, Song, Ohwaki, Kenji, Gaur, Vidhi, Long, Yun Chau, Hargreaves, Mark, McGee, Sean L and Kusunoki, Jun 2012, Histone deacetylase 5 regulates glucose uptake and insulin action in muscle cells, Journal of molecular endocrinology, vol. 49, no. 3, pp. 203-201.

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Title Histone deacetylase 5 regulates glucose uptake and insulin action in muscle cells
Author(s) Raichur, Suryaprakash
Hooi-Teh, Song
Ohwaki, Kenji
Gaur, Vidhi
Long, Yun Chau
Hargreaves, Mark
McGee, Sean L
Kusunoki, Jun
Journal name Journal of molecular endocrinology
Volume number 49
Issue number 3
Start page 203
End page 201
Total pages 9
Publisher Society for Endocrinology
Place of publication Bristol, England
Publication date 2012-12-01
ISSN 0952-5041
1479-6813
Keyword(s) cell metabolism
controlled study
gene silencing
glucose metabolism
glucose transport
glycogen synthesis
human cell
muscle cell
muscle metabolism
protein expression
Summary 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.
Language eng
Field of Research 111699 Medical Physiology not elsewhere classified
Socio Economic Objective 920104 Diabetes
HERDC Research category C1 Refereed article in a scholarly journal
Persistent URL http://hdl.handle.net/10536/DRO/DU:30050129

Document type: Journal Article
Collection: School of Medicine
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