The mitochondrial antioxidant MitoQ alleviates oxidative stress, endoplasmic reticulum stress and mitochondrial function in pancreatic β cells under hyperglycaemic conditions

MitoQ can exhibit protective effects against oxidative damage. The increase in ROS production during glucose metabolism in β cells is exacerbated under hyperglycaemic conditions such as type 2 diabetes (T2D), thus constituting a key contributor to β cell function impairment. Our aim was to evaluate the effect of MitoQ on oxidative stress, endoplasmic reticulum (ER) stress and NFκB signalling in a pancreatic β cell line under normoglycaemia (NG, 11.1 mM) and hyperglycaemia (HG, 25 mM). We employed the β cell line INS-1E treated with or without MitoQ (0.5 µM) under NG or HG conditions and assessed the following parameters: O 2 consumption, mitochondrial function, oxidative stress, calcium, ER stress markers and NFκB-p65. MitoQ prevented the enhanced ROS production and O 2 consumption and reduced GSH levels normally present under HG. MitoQ decreased ER stress markers (GRP78 and P-eif2α) and NFκB-p65, both of which increased under HG. These findings suggest that MitoQ treatment modulates oxidative stress and mitochondrial function, thereby ameliorating ER stress and NFκB activation. In this way, it possesses potential benefits as a treatment for insulin resistance-related diseases such as T2D.