Abstract
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.
Original language | English |
---|---|
Journal | Molecular Medicine |
Volume | 17 |
Issue number | 5-6 |
Pages (from-to) | 378-90 |
Number of pages | 13 |
ISSN | 1076-1551 |
DOIs | |
Publication status | Published - May 2011 |