Epigenetics Variation and Pathogenesis in Diabetes.

Haichen Zhang, Toni I Pollin

Journal: Current diabetes reports 2019;18(11):121

PMID: 30280270

Abstract

PURPOSE OF REVIEW

Great strides have recently been made in elucidating the role of genetic sequence variation in diabetes pathogenesis. Increasingly, studies are focusing on other factors that may contribute to the pathogenesis of diabetes, such as epigenetics, a term "traditionally" encompassing changes to the DNA that do not alter sequence and are heritable (primary methylation and histone modification) but often expanded to include microRNAs. This review summarizes latest findings on the role of epigenetics in diabetes pathogenesis.

RECENT FINDINGS

Recent studies illustrate roles for methylation changes, histone modification, imprinting, and microRNAs across several diabetes types and complications. Notably, methylation changes in the human leukocyte antigen (HLA) region have been found to precede the development of type 1 diabetes. In type 2 diabetes, lifestyle factors appear to interact with epigenetic mechanisms in pathogenesis. Emerging technologies have allowed increasingly comprehensive descriptive analysis of the role of epigenetic mechanisms in diabetes pathogenesis which have yielded meaningful insights into effects on expression of relevant genes. These findings have the potential to inform future development of predictive testing to enable primary prevention and further work to uncover the complex pathogenesis of diabetes.

Address: Department of Medicine, Division of Endocrinology, Diabetes and Nutrition Program for Personalized and Genomic Medicine, University of Maryland School of Medicine, 670 West Baltimore Street, Room 4040, Baltimore, MD, 21201, USA.; Department of Medicine, Division of Endocrinology, Diabetes and Nutrition Program for Personalized and Genomic Medicine, Department of Epidemiology and Public Health, University of Maryland School of Medicine, 670 West Baltimore Street, Room 4040, Baltimore, MD, 21201, USA. [email protected].

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