Epigenetics of diabetes Type 2 have shown that miRNAs have pivotal roles in many different gene regulatory pathways. A subset of miRNAs has been shown to be involved in metabolic regulation of glucose homeostasis and in epigenetics of diabetes type 2. Pancreatic islet-specific miR-375 inhibits insulin secretion in mouse pancreatic β-cells by inhibiting the expression of the protein myotrophin. An overexpression of miR-375 can completely suppress glucose-induced insulin secretion, while inhibition of native miR-375 will increase insulin secretion. In another study, increasing the level of miR-9, a different miRNA, resulted in a severe defect in glucose-stimulated insulin release. This happens because miR-9 down-regulated the transcription
Epigenetics of diabetes Type 2 the C677t mutation. This is not a spontaneous mutation; it is actually hereditary. While the mutation does not inactivate the gene, it greatly reduces the efficiency, thus impairing the formation of methionine. The lack of this amino acid prevents methylation from occurring, and as said above, hypomethylation leads to increased susceptibility to Type 2 Diabetes. Type 2 diabetes associated sequence polymorphisms have been identified in 30 linkage disequilibrium (LD) blocks across the human genome, but their effects only explain a minor fraction of the observed phenotypic diversity among individuals. Previously, in other studies it has been demonstrated that connections between