Endoplasmic Reticulum Stress in the β-Cell Pathogenesis of Type 2 Diabetes

Type 2 diabetes is a complex metabolic disorder characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency by beta-cell failure. Even if the mechanisms underlying the pathogenesis of beta-cell failure are still under investigation, recent increasing genetic, experimental, and clinical evidence indicate that hyperactivation of the unfolded protein response (UPR) to counteract metabolic stresses is closely related to beta-cell dysfunction and apoptosis. Signaling pathways of the UPR are a double-edged sword that can promote adaptation or apoptosis depending on the nature of the ER stress condition. In this paper, we summarized our current understanding of the mechanisms and components related to ER stress in the beta-cell pathogenesis of type 2 diabetes.