Figure 1.

K_ATP channels are neuroprotective and sulfonylurea use can exacerbate ischemia-induced brain damage. In the pancreatic β, K_ATP channels serve as a metabolic sensor to post-prandial glucose metabolism. The closure of K_ATP channels depolarizes cell membrane, activates voltagegated calcium channels (VGCCs) and thus leads to insulin release. In the diabetic patients, sulfonylureas can be used to block K_ATP channels and increase insulin release. In an ischemic neuron, the reduction in ATP: ADP ratio opens K_ATP channels, lowering membrane potential and stabilizing the membrane, thus reducing cell excitotoxicity. In other words, the opening of K_ATP channels is neuroprotective. In the diabetic patients using sulfonylureas, the neuroprotective effects of K_ATP channels neuroprotective effects are abolished.