PPARG and Hyperglycemia: Hyperglycemia activates PPARγ pathways, thus decreasing the invasion of human CTB, followed by the increase of IL-6 and soluble fms-like tyrosine kinase-1 (sFIt-1) and the inhibition of urokinase plasminogen activator (uPA) and plasminogen activator inhibitor 1 (PAI-1) [93].