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
Genetic causes of diabetes mellitus type 2 genes, and these differences in the nucleotide sequences alter phenotypic traits that exhibit increased susceptibility to the diabetes. GWAS has revealed 65 different loci (where single nucleotide sequences differ from the patient and control group's genomes), and genes associated with type 2 diabetes, including "TCF7L2", "PPARG", "FTO", "KCNJ11","NOTCH2", "WFS1", "IGF2BP2", "SLC30A8", "JAZF1", "HHEX, DGKB, CDKN2A, CDKN2B, KCNQ1, HNF1A, HNF1B MC4R, GIPR, HNF4A, MTNR1B, PARG6, ZBED3, SLC30A8, CDKAL1, GLIS3, GCKR," among others."KCNJ11" (potassium inwardly rectifying channel, subfamily J, member 11), encodes the islet ATP-sensitive potassium channel Kir6.2, and "TCF7L2" (transcription factor 7–like 2) regulates proglucagon gene expression and thus the production