Epigenetics of diabetes Type 2 Since Type 2 diabetes is characterized by chronic hyperglycaemia as a result of impaired pancreatic beta cell function and insulin resistance in peripheral tissues, it was thought that the gene might be downregulated in type 2 diabetes patients through DNA methylation. The defects in pancreatic beta cell function and insulin resistance in peripheral tissues were thought to be the result of impaired ATP production from reduced oxidative phosphorylation. It was found that the mRNA expression of PPARGC1A was markedly reduced in pancreatic islets from type 2 diabetic donors compared with that of non-diabetic donors. Using bisulfite testing, it was also
Epigenetics of diabetes Type 2 left behind during both HCNE-driven expression and IRX3 expression. In summary, persons at high risk for Type 2 Diabetes and obesity have a highly methylated 7.7 kb region in the linkage disequilibrium block of the FTO gene. This methylation leads to the deactivation of the HCNE located within it, and decreased IRX3 expression. When IRX3 was knocked out, there was a drop in the number of β-cells that produce insulin and the α-cells that produce glucagon. This sudden drop indicates a direct relationship between the FTO gene, IRX3, and Type 2 diabetes. Epigenetics of diabetes Type 2 In recent years