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Article

Acute sulfonylurea therapy at disease onset can cause permanent remission of KATP-induced diabetes.

Diabetes - 1 Oct 2011

Remedi Maria Sara, Agapova Sophia E, Vyas Arpita K, Hruz Paul W, Nichols Colin G

Abstract excerpt

OBJECTIVE: Neonatal diabetes mellitus (NDM) can be caused by gain-of-function ATP-sensitive K(+) (K(ATP)) channel mutations. This realization has led to sulfonylurea therapy replacing insulin injections in many patients. In a murine model of K(ATP)-dependent NDM, hyperglycemia and consequent loss of β-cells are both avoided by chronic sulfonylurea treatment. Interestingly, K(ATP) mutations may underlie...

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Identifiers

PMID: 21813803
DOI: 10.2337/db11-0538
PMCID: PMC3178299

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Acute sulfonylurea therapy at disease onset can cause permanent remission of KATP-induced diabetes.PMID 21813803Read ↗

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Effectiveness and safety of long-term treatment with sulfonylureas in patients with neonatal diabetes due to KCNJ11 mutations: an international cohort study.Semantic proximity Read ↗

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Sur1 Knockout MiceSemantic proximity Read ↗

An ATP-binding mutation (G334D) in KCNJ11 is associated with a sulfonylurea-insensitive form of developmental delay, epilepsy, and neonatal diabetes.Semantic proximity Read ↗

Inactivating the permanent neonatal diabetes gene Mnx1 switches insulin-producing β-cells to a δ-like fate and reveals a facultative proliferative capacity in aged β-cellsSemantic proximity Read ↗

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Expression of an activating mutation in the gene encoding the KATP channel subunit Kir6.2 in mouse pancreatic beta cells recapitulates neonatal diabetes.Semantic proximity Read ↗

The G53D mutation in Kir6.2 (KCNJ11) is associated with neonatal diabetes and motor dysfunction in adulthood that is improved with sulfonylurea therapy.Semantic proximity Read ↗

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