Evolution of diabetes: plasticity of epigenetic is a novel key to cause t2dm

Susmit Kosta*, C. B.S. Dangi, Banerjee N., Manpreet Kaur

Abstract


Epigenetic modification of gene expression is one mechanism by which genetic susceptibility and environmental insults can lead to Type 2 Diabetes Mellitus (T2DM) problem worldwide. The peripheral insulin resistance is common during obesity and aging in animals and people, progression to T2DM is largely due to insulin secretory dysfunction and significant apoptosis of functional β-cells, leading to an inability to compensate for insulin resistance. It is recognized that environmental factors and genetic play an important role in the pathogenesis of diabetes. However, our knowledge surrounding molecular mechanisms by which these factors trigger β-cell dysfunction and diabetes is still limited. Epigenetic changes could account for the accelerated rates of chronic and persistent phenotype and genotype complications associated with diabetes. Epigenetic mechanisms are likely involved, especially in obesity and diabetes mellitus. It is not the only factor; there is a wide variety of potential modulators of the human epigenome which can be modified through phenotype and genotype. Epigenetic changes are defined as mitotically inheritable alterations in gene expression that are not related to changes in DNA sequence. In this article, we comprehensively review the role of UV radiation, DNA methylation, histone modifications and MicroRNA (miRs) effects in glucose metabolism in health and disease. It  also address to understand epigenetic phenomena, which is directly attributable to technologies that allow researchers to pinpoint the genomic location of proteins package, and molecular events which underlie transcriptional changes or regulate access to DNA for the management of T2DM.

Keywords


Type 2 Diabetes Mellitus (T2DM); Epigenetic.

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DOI: http://dx.doi.org/10.21746/ijbio.2013.12.0013

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