On the other hand, as observed in T2DM patients, a decline of cardiac function and increased myocardial hypertrophy, fibrosis, and steatosis were predominantly found in PPARα [105, 106], PPARγ [107, 108], long-chain acyl-CoA synthetase-1 (LCACS1) [109, 110], lipoprotein lipase (LPL) [111, 112], and fatty acid transport protein-1 (FATP1) [113, 114] overexpressed mice. This evidence concerns the gene LPL and type 2 diabetes mellitus.