DNA methylation analysis of the proinflammatory IL6 gene in Type 2 Diabetespatients

Type 2 diabetes (T2D) is a metabolic disorder, characterized by progressive dysfunction of pancreatic β-cells and insulin resistance, resulting from impaired insulin signaling. The prevalence of T2D is rising sharply in association with increases in obesity. Obesity-induced T2D is recognized as an auto-inflammatory disease. A state of chronic low-grade inflammation promoted by obesity, which is reflected by an increased production of pro-inflammatory cytokines, may contribute to the development of T2D. Many studies now converge to show that several cytokines, such as IL-1β and IL-6 contribute to the pathology and physiology of T2D through their interaction with insulin signaling pathways and β-cell function.Type 2 diabetes is the result of interaction between epigenetic factors and a strong hereditary component. Epigenetics has been defined as the study of changes in gene function that are heritable and that do not entail a change in DNA sequence . The aim of this casecontrol study, was to investigate the changes in methylation pattern of IL-6 in peripheral blood mononuclear cells from individuals with normal (n = 15), moderately high (n = 15), and high (n =15) blood glucose levels, using bisulfite sequencing. Considering IL6 dual pre- and anti-inflammation behavior in the inflammation, there was not a significant change in methylation pattern of IL-6 in individuals with diabetes and pre-diabetes compared with controls

Keywords:

Methylation , Diabetes , Inflammation