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RESEARCH PRODUCT

Epigenetics, oxidative states and diabetes

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Abstract Although controlling a wide range of physiological cell functions, redox states unbalance during inflammation toward oxidative stress. Specific regions of our genome are extremely sensitive to both oxygen and reactive oxygen species, therefore modulating gene transcription in response to this specific epigenetic effect. Additional epigenetic mechanisms may include the alteration of the methylation states of DNA, protein and lipid nitration or modulation of specific microRNAs. A crucial role in finely tuning redox states is also played by mitochondria, where oxidative phosphorylation is epigenetically controlled. Diabetes, the most considerable “epigenetic” clinical disorder, exacerbates metabolic redox states, generating oxidative stress. Although the precise molecular mechanisms are far to be fully elucidated, it is clear that oxidative stress, genome and diabetes are interconnected by epigenetics. In this chapter, we will strictly focus on the cause–effect relationship between redox states and epigenetics and how these modifications represent the biological foundation by which diabetes originates and evolves.