ABSTRACT
ATP-sensitive K+ (KATP) channels couple changes in pancreatic β-cell metabolism to changes in their electrical excitability, allowing them to fire action potentials and secrete insulin. KATP channels are heterooctamers, comprising four inwardly rectifying K+ (Kir) channel subunits and four accessory sulfonylurea receptor subunits. Metabolic sensitivity is conferred upon KATP by 12 ATP/ADP-binding sites (one on each Kir subunit and two on each accessory subunit). Given its central role in β-cell physiology, it is not surprising that mutations in the genes encoding either subunit of KATP cause diseases of insulin secretion. This chapter provides a brief overview of the role KATP plays in β-cell physiology, the structural and molecular basis for its metabolic sensitivity, and the pathology and treatment of the diseases that arise from its dysfunction.
