In this condition, myocardial metabolism is switched to FA uptake and oxidation.33 Therefore, diabetic heart is subjected to excessive oxidative stress, inflammation and lipotoxiciy that contribute to insulin resistance, functional impairment of the mitochondria, cardiomyocyte hypertrophy, apoptosis and dysregulation of autophagic activity.34 Vildagilptin, as an enhancer of GLP1 hormone, increased plasma levels of insulin, decreased glucose intolerance and HOMA1-IR, so increased insulin sensitivity in our type-II diabetic rats. The gene discussed is INS; the disease is Glucose intolerance.