| Literature DB >> 26044585 |
Dustin E Schones1, Amy Leung2, Rama Natarajan2.
Abstract
The incidence of obesity across the globe has doubled over the past several decades, leading to escalating rates of diabetes mellitus, cardiovascular disease, and other complications. Given this dramatic rise in disease incidence, understanding the cause of these diseases is therefore of paramount importance. Metabolic diseases, such as obesity and diabetes mellitus, result from a multitude of genetic and environmental factors. Although the genetic basis of these diseases has been extensively studied, the molecular pathways whereby environmental factors influence disease progression are only beginning to be understood. One manner by which environmental factors can contribute to disease progression is through modifications to chromatin. The highly structured packaging of the genome into the nucleus through chromatin has been shown to be fundamental to tissue-specific gene regulation. Modifications to chromatin can regulate gene expression and are involved in a myriad of biological functions, and hence, disruption of these modifications is central to many human diseases. These modifications can furthermore be epigenetic in nature, thereby contributing to prolonged disease risk. Recent work has demonstrated that modifications to chromatin are associated with the progression of both diabetes mellitus and obesity, which is the subject of this review.Entities:
Keywords: chromatin; diabetes mellitus; epigenomics; gene–environment interaction; obesity
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Year: 2015 PMID: 26044585 PMCID: PMC4482788 DOI: 10.1161/ATVBAHA.115.305041
Source DB: PubMed Journal: Arterioscler Thromb Vasc Biol ISSN: 1079-5642 Impact factor: 8.311