Further, the associated glucotoxicity, lipotoxicity, inflammation, oxidative stress, and hyperinsulinemia in T2DM combine to activate 5′ AMP-activated protein kinase (AMPK) and mammalian target of rapamycin complex 1 (mTORC1), which impairs mitophagy via mTORC1 to cause phosphorylation of Unc51-like kinase, hATG1 (ULK1) [101]. Here, ULK1 is linked to hyperinsulinism.