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Successful oral sulfonylurea treatment for diabetes caused by Kir6.2 mutations

Nature Clinical Practice Endocrinology & Metabolism volume 2, pages 652–653 (2006)Cite this article

Pearson ER et al. (2006) Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations. N Engl J Med 355: 467–477

KCNJ11 encodes the Kir6.2 subunit of the ATP-sensitive inward-rectifier potassium channel (IKATP). Patients with KCNJ11 mutations exhibit marked hyperglycemia within the first 6 months of life, because their β-cell IKATP channels do not close when intracellular ATP levels rise in response to glucose metabolism. Open IKATP channels cause membrane hyperpolarization that keeps voltage-gated calcium channels closed, and prevents insulin release. Sulfonylureas bind to the SUR1 regulatory subunit of IKATP channels and could, therefore, close mutated IKATP channels through a non-ATP-dependent route.

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Successful oral sulfonylurea treatment for diabetes caused by Kir6.2 mutations. Nat Rev Endocrinol 2, 652–653 (2006). https://doi.org/10.1038/ncpendmet0331

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