@entity14625 Impairs Insulin Secretion of Pancreatic b-Cells through Increased Production of ROS and Mitochondrial Dysfunction Mediated by Upregulation of XXXX and MAPKs.

@entity14625 @entity6 @entity26 @entity898 @entity74 @entity5912 @entity1435 @entity413 @entity855
@entity14625 (MG) is a highly reactive @entity413 metabolic intermediate and a major precursor of advanced glycation end products. MG level is elevated in @entity74 such as @entity6 . Substantial evidence has shown that MG is involved in the pathogenesis of @entity6 and @entity6 complications. We investigated the impact of MG on insulin secretion by MIN6 and INS-1 cells and the potential mechanisms of this effect. Our study demonstrates that MG impaired insulin secretion by MIN6 or ISN-1 cells in a dose-dependent manner. It increased reactive @entity26 species (ROS) production and apoptosis rate in MIN6 or ISN-1 cells and inhibited mitochondrial membrane potential (MMP) and @entity855 production. Furthermore, the expression of @entity5912 , JNK, and @entity1435 as well as the phosphorylation JNK and @entity1435 was increased by MG. These effects of MG were attenuated by MG scavenger @entity898 . Collectively, these data indicate that MG impairs insulin secretion of pancreatic b-cells through increasing ROS production. High levels of ROS can damage b-cells directly via JNK/ @entity1435 upregulation and through activation of @entity5912 resulting in reduced MMP and @entity855 production, leading to b-cell dysfunction and impairment of insulin production.
