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Article

[Glycemic index of meals and postprandial glycemia in patients with permanent neonatal diabetes due to Kir6.2 gene mutations].

Przeglad lekarski - 1 Jan 2007

Klupa Tomasz, Małecki Maciej, Skupień Jan, Szalecki Mieczysław, Jałowiec Irena, Surdej Barbara, Myśliwiec Małgorzata, Sieradzki Jacek

Abstract excerpt

Activating mutations in the KCNJ11 gene encoding the ATP-sensitive potassium-channel subunit of Kir6.2 result in the phenotype of permanent neonatal diabetes (PNDM). Patients with PNDM can be successfully transferred from insulin to sulphonylurea. It is not clear, however, whether the type of die...

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Share to Blood Glucose
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hypoglycemic Agents

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Share to Potassium Channels, Inwardly Rectifying

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Source

Identifiers

PMID: 18159846

Genes

KCNJ11

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-18159846-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

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[Glycemic index of meals and postprandial glycemia in patients with permanent neonatal diabetes due to Kir6.2 gene mutations].PMID 18159846Read ↗

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[Low doses of sulphonyluria as a successful replacement for insulin therapy in a patient with neonatal diabetes due to a mutation of KCNJ11 gene encoding Kir6.2].Semantic proximity Read ↗

Sulfonylurea treatment outweighs insulin therapy in short-term metabolic control of patients with permanent neonatal diabetes mellitus due to activating mutations of the KCNJ11 (KIR6.2) geneSemantic proximity Read ↗

Familial permanent neonatal diabetes with KCNJ11 mutation and the response to glyburide therapy--a three-year follow-up.Semantic proximity Read ↗

Diabetes and hypoglycaemia in young children and mutations in the Kir6.2 subunit of the potassium channel: therapeutic consequences.Semantic proximity Read ↗

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