The importance of K(ATP) channels in stimulus-secretion coupling of β-cells is well established, although they are not indispensable for the maintenance of glycaemic control. This review article depicts a new role for K(ATP) channels by showing that genetic or pharmacological ablation of these channels protects β-cells against oxidative stress. Increased production of oxidants is a crucial factor in the pathogenesis of type 2 diabetes mellitus (T2DM). T2DM develops when β-cells can no longer compensate for the high demand of insulin resulting from excess fuel intake. Instead β-cells start to secrete less insulin and β-cell mass is diminished by apoptosis. Both, reduction of insulin secretion and β-cell mass induced by oxidative stress, are prevented by deletion or inhibition of K(ATP) channels. These findings may open up new insights into the early treatment of T2DM.
© 2012 Blackwell Publishing Ltd.