Abstract
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by hyperglycaemia, which can cause micro- and macrovascular complications. Chronic inflammation may be the cause and result of T2DM, and its related complications as an imbalance between pro- and anti-inflammatory cytokines can affect immune functions. Apart from genetic changes occurring within the body resulting in inflammation in T2DM, epigenetic modifications can modify gene expression in response to environmental cues such as an unhealthy diet, lack of exercise and obesity. The most widely studied epigenetic modification, DNA methylation (DNAm), regulates gene expression and may manipulate inflammatory genes to increase or decrease inflammation associated with T2DM. This review explores the studies related to epigenetic changes, more specifically DNAm, associated with chronic inflammation in T2DM, at both the cell and tissue levels. Studying epigenetic alterations during inflammatory response, as a result of genetic and environmental signals, creates opportunities for the development of "early detection/relative risk" tests to aid in prevention of T2DM. Understanding inflammation in T2DM at the gene level in inflammation-associated cells and tissues may provide further insight for the development of specific therapeutic targets for the disorder.
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