The regulation of a K⁺ current activating during oscillatory electrical activity (I_K,slow) in an insulin‐releasing β‐cell was studied by applying the perforated patch whole‐cell technique to intact mouse pancreatic islets. The resting whole‐cell conductance in the presence of 10 mm glucose amounted to 1.3 nS, which rose by 50 % during a series of 26 simulated action potentials. Application of the K_ATP‐channel blocker tolbutamide produced uninterrupted action potential firing and reduced I_K,slow by ≈50 %. Increasing glucose from 15 to 30 mm, which likewise converted oscillatory electrical activity into continuous action potential firing, reduced I_K,slow by ≈30 % whilst not affecting the resting conductance. Action potential firing may culminate in opening of K_ATP channels by activation of ATP‐dependent Ca²⁺ pumping as suggested by the observation that the sarco‐endoplasmic reticulum Ca²⁺‐ATPase (SERCA) inhibitor thapsigargin (4 μm) inhibited I_K,slow by 25 % and abolished bursting electrical activity. We conclude that oscillatory glucose‐induced electrical activity in the β‐cell involves the opening of K_ATP‐channel activity and that these channels, in addition to constituting the glucose‐regulated K⁺ conductance, also play a role in the graded response to supra‐threshold glucose concentrations.