Figure 3.

Cellular mechanisms in pancreatic β-cells involving mitochondrial ROS generation and their implication in insulin release and diabetes onset. (A) Mechanism of insulin release in β-cells in normal conditions. (B) Impaired insulin release by β-cells under hyperglycemic conditions. High glucose concentration in blood implies high ROS generation by mitochondria leading to alterations in insulin release. (C) Scheme of how hyperglycemia promotes ROS generation by ETC (electron transport chain) in mitochondria inducing oxidative stress. Oxidative stress is boosted by the ER stress as consequence of the accumulation of unfolded insulin peptides due to the enhanced demand of this hormone. In addition, the implication of Ca²⁺ ions from ER as a factor that increases ROS in mitochondria and the interconnection of both organelles through MAM (mitochondria-associated ER membranes) are depicted. ATP: Adenosine triphosphate; ER: Endoplasmic reticulum; GLUT2: Glucose transporter-2; ROS: Reactive oxygen species.