In this study, treatment with glucose or insulin decreased the expression of TET2, but treatment with fatty acids did not influence the expression of TET2. These results suggest that hyperinsulinemia and hyperglycemia, observed in patients with visceral fat obesity, may decrease the expression of TET2. AMPK, which is a key regulator as an energy sensor for maintaining homeostasis, is inactivated in hyperglycemic conditions and activated upon energy stress induced by ATP depletion, such as in hypoglycemia and hypoxia33,34. Here, TET2 is linked to Hyperglycemia.