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 re-methylated to form methionine, be taken into the cysteine biosynthetic pathway, or be freed into the extracellular medium. When a person lacks sulfur in their diet, it prompts the body to use methionine and form cysteine. This in turn increases the risk of a person contracting type 2 diabetes later in life. The reason behind this turns out to be rather simple. Methionine directly affects S-adenosyl methionine (SAM) levels. SAM is the substance that provides the methyl groups for DNA methylation. A shortage of SAM leads to an inability to develop proper methylation patterns, and is thought to be an