Methylglyoxal Impairs Insulin Secretion of Pancreatic β-Cells through Increased Production of ROS and Mitochondrial Dysfunction Mediated by Upregulation of UCP2 and MAPKs

Figure 9

Schematic representation of proposed signaling pathways suggested by the results of this study. Methylglyoxal increases production of reactive oxygen species (ROS), which then reduces the mitochondrial membrane potential (MMP) and ATP production via UCP2 upregulation. UCP2 upregulation in turn leads to β-cell damage and, ultimately, impairment of insulin secretion. ROS also may induce β-cell damage and impair insulin secretion directly via upregulation of MAPKs (JNK/P38).