In other words, diabetes may lead to the activation of Akt/mTORC1 and the inhibition of SIRT1/PGC-1α/FGF21 through hyperinsulinemia, thereby inhibiting autophagic flux and promoting oxidative stress and mitochondrial dysfunction of diabetic myocardial cells, and thus promoting pathological cardiac hypertrophy. Here, AKT1 is linked to cardiac hypertrophy.