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
Diabetes mellitus type 2 2 diabetes. Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance. Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver, and fat tissue. In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood. The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance