 Under resting conditions, the weakly inwardly rectifying KATP channels in pancreatic beta cells are spontaneously active, allowing potassium ions to flow out of the cell and maintaining a negative resting membrane potential (slightly more positive than the K+ reversal potential).In the presence of higher glucose metabolism, and consequently increased relative levels of ATP, the KATP channels close, causing the membrane potential of the cell to depolarize, activating voltage-gated calcium channels, and thus promoting the calcium-dependent release of insulin.The change from one state to the other happens quickly and synchronously, due to C-terminus multimerization among proximate KATP channel molecules.