Laurence Ladrière

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 concluded that apoptosis is the main mode of FFA- and cytokine-induced beta-cell death but the mechanisms involved are different, suggesting that FFAs trigger an endoplasmic reticulum (ER) stress response through an NF-kappaB- and nitric oxide-independent mechanism.

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: In this paper, the authors used RNA sequencing to map transcripts expressed in five palmitate-treated human islet preparations, observing 1,325 modified genes, including PAX4 and GATA6.

TL;DR: The observations suggest that GLP-1 agonists increase in a context-dependent way the β-cell defense mechanisms against different pathways involved in ER stress–induced apoptosis, which allows for targeted approaches to alleviate β- cell ER stress in diabetes.