Switching from Insulin to Oral Sulfonylureas in Patients with Diabetes Due to Kir6.2 Mutations | Zendy

Ewan R. Pearson | Zendy; Isabelle Flechtner | Zendy; Pål R. Njølstad | Zendy; Maciej T. Małecki | Zendy; Sarah E. Flanagan | Zendy; Brian Larkin | Zendy; Frances M. Ashcroft | Zendy; I Klimeś | Zendy; Ethel Codner | Zendy; Violeta Iotova | Zendy; Annabelle S. Slingerland | Zendy; Julian HamiltonShield | Zendy; JeanJacques Robert | Zendy; Jens J. Holst | Zendy; Penny Clark | Zendy; Sian Ellard | Zendy; Oddmund Søvik | Zendy; Michel Polak | Zendy; Andrew T. Hattersley | Zendy

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Switching from Insulin to Oral Sulfonylureas in Patients with Diabetes Due to Kir6.2 Mutations

Author(s) -

Ewan R. Pearson,

Isabelle Flechtner,

Pål R. Njølstad,

Maciej T. Małecki,

Sarah E. Flanagan,

Brian Larkin,

Frances M. Ashcroft,

I Klimeś,

Ethel Codner,

Violeta Iotova,

Annabelle S. Slingerland,

Julian HamiltonShield,

JeanJacques Robert,

Jens J. Holst,

Penny Clark,

Sian Ellard,

Oddmund Søvik,

Michel Polak,

Andrew T. Hattersley

Publication year - 2006

Publication title -

new england journal of medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 19.889

H-Index - 1030

eISSN - 1533-4406

pISSN - 0028-4793

DOI - 10.1056/nejmoa061759

Subject(s) - sulfonylurea , medicine , tolbutamide , endocrinology , insulin , sulfonylurea receptor , diabetes mellitus , kir6.2 , glibenclamide , glucagon , glycemic , type 2 diabetes , biology , protein subunit , biochemistry , gene

Heterozygous activating mutations in KCNJ11, encoding the Kir6.2 subunit of the ATP-sensitive potassium (K(ATP)) channel, cause 30 to 58 percent of cases of diabetes diagnosed in patients under six months of age. Patients present with ketoacidosis or severe hyperglycemia and are treated with insulin. Diabetes results from impaired insulin secretion caused by a failure of the beta-cell K(ATP) channel to close in response to increased intracellular ATP. Sulfonylureas close the K(ATP) channel by an ATP-independent route.

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