A series of experiments further revealed that LEAP-2 regulates insulin secretion and glucose metabolism by binding to the receptor GHSR1a and influencing downstream peroxidase proliferator-activated receptor γ (PPARγ) and glucokinase (Gck) expression levels, providing usable targets for the treatment of type 2 diabetes (T2D) [62,63]. This evidence concerns the gene PPARG and type 2 diabetes mellitus.