Endoplasmic Reticulum Stress in theβ-Cell Pathogenesis of Type 2 Diabetes

Abstract

Type 2 diabetes is a complex metabolic disorder characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency byβ-cell failure. Even if the mechanisms underlying the pathogenesis ofβ-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 toβ-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 theβ-cell pathogenesis of type 2 diabetes.