ATP-sensitive potassium (KATP) channels are inhibited by intracellular ATP and activated by ADP. Nutrient oxidation in β-cells leads to a rise in [ATP]-to-[ADP] ratios, which in turn leads to reduced KATP channel activity, depolarization, voltage-dependent Ca2+ channel activation, Ca2+ entry, and exocytosis. Persistent hyperinsulinemic hypoglycemia of infancy (HI) is a genetic disorder characterized by dysregulated insulin secretion and, although rare, causes severe mental retardation and epilepsy if left untreated. The last five or six years have seen rapid advance in understanding the molecular basis of KATP channel activity and the molecular genetics of HI. In the majority of cases for which a genotype has been uncovered, causal HI mutations are found in one or the other of the two genes, SUR1 and Kir6.2, that encode the KATP channel. This article will review studies that have defined the link between channel activity and defective insulin release and will consider implications for future understanding of the mechanisms of control of insulin secretion in normal and diseased states.

Original languageEnglish
Pages (from-to)E207-E216
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Issue number2 46-2
StatePublished - 2002


  • ATP-sensitive potassium
  • Diabetes
  • Hyperinsulinemic hypoglycemia of infancy
  • Kir6.2
  • Pancreas
  • SUR1


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