It has been shown that azilsartan reduced left ventricular hypertrophy, cardiac fibrosis, plasminogen activator inhibitor-1 (PAI-1; a marker of profibrosis) in aortic banding mice fed high-fat diet [55], indicating that azilsartan may exert favorable biological effects in non-diabetic obese insulin-resistant condition, which shares a common mechanism such as enhanced ROS/inflammation signals with the current model. This evidence concerns the gene INS and left ventricular hypertrophy.