Paul Hekerman

TL;DR: Saturated FFA induce ER stress via ER Ca2+ depletion and the IRE1 and resulting JNK activation contribute to β-cell apoptosis, suggesting that ER stress in primary β-cells is primarily lipotoxic, and not glucolipotoxic.

TL;DR: It is demonstrated that excessive eIF2α phosphorylation is poorly tolerated by β-cells and exacerbates free fatty acid-induced apoptosis, which modifies the present paradigm regarding the beneficial role of eIF 2 α phosphorylated cells and must be taken into consideration when designing therapies to protect β- cells in type 2 diabetes.

TL;DR: Cytokines activate the PPAR-δ gene network in beta cells, but this network does not regulate the pro-inflammatory response to cytokines because beta cells lack constitutive BCL-6 expression, which may render beta cells particularly susceptible to propagating inflammation in type 1 diabetes.

TL;DR: In this paper, Salubrinal selectively inhibitseIF2 dephosphorylation, protecting other cells against endo-plasmic reticulum stress-mediated apoptosis, and has beenproposed as a -cell protector.