Chronic treatment with valproate protects INS1 cell from palmitate-induced ER stress and apoptosis by inhibiting GSK3β

Objective Reduction of b-cell mass is increasingly recognized as one of the main contributing factors to the pathogenesis of type 2 diabetes. Chronic free fatty acid (FFA) exposure has been shown to induce endoplasmic reticulum (ER) stress that may contribute to promoting pancreatic b-cell apoptosis. In the present study, we first investigated whether anticonvulsant sodium valproate (VPA), at clinically relevant doses, protects pancreatic b-cell from palmitate-induced apoptosis and the mechanism underlying anti-apoptosis.