AKT1 Regulates Endoplasmic Reticulum Stress and Mediates the Adaptive Response of Pancreatic <i>β</i> Cells
Zhechu Peng, Richa Aggarwal, Ni Zeng, Lina He, Eileen X. Stiles, Anketse Debebe, Jingyu Chen, Chien-Yu Chen, Bangyan L. Stiles
Abstract
proliferated as a compensatory mechanism for metabolic overload. Similar effects were not observed in βA1KO mice. We further demonstrated that AKT1 protein deficiency caused endoplasmic reticulum (ER) stress and potentiated β cells to undergo apoptosis. Our results revealed that AKT1 protein loss led to the induction of eukaryotic initiation factor 2 α subunit (eIF2α) signaling and ER stress markers under normal-chow-fed conditions, indicating chronic low-level ER stress. Together, these data established a role for AKT1 as a growth and survival factor for adaptive β-cell response and suggest that ER stress induction is responsible for this effect of AKT1.