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Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus

Both common forms of diabetes have an inflammatory pathogenesis in which immune and metabolic factors converge on interleukin-1β as a key mediator of insulin resistance and β-cell failure. In addition to improving insulin resistance and preventing β-cell inflammatory damage, there is evidence of gen...

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Bibliographic Details
Published in:Molecular medicine (Cambridge, Mass.) Mass.), 2011-05, Vol.17 (5-6), p.378-390
Main Authors: Christensen, Dan P, Dahllöf, Mattias, Lundh, Morten, Rasmussen, Daniel N, Nielsen, Mette D, Billestrup, Nils, Grunnet, Lars G, Mandrup-Poulsen, Thomas
Format: Article
Language:English
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Summary:Both common forms of diabetes have an inflammatory pathogenesis in which immune and metabolic factors converge on interleukin-1β as a key mediator of insulin resistance and β-cell failure. In addition to improving insulin resistance and preventing β-cell inflammatory damage, there is evidence of genetic association between diabetes and histone deacetylases (HDACs); and HDAC inhibitors (HDACi) promote β-cell development, proliferation, differentiation and function and positively affect late diabetic microvascular complications. Here we review this evidence and propose that there is a strong rationale for preclinical studies and clinical trials with the aim of testing the utility of HDACi as a novel therapy for diabetes.
ISSN:1076-1551
1528-3658
1528-3658
DOI:10.2119/molmed.2011.00021