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Article

The prevalent Glu23Lys polymorphism in the potassium inward rectifier 6.2 (KIR6.2) gene is associated with impaired glucagon suppression in response to hyperglycemia.

Diabetes - 1 Sept 2002

Tschritter Otto, Stumvoll Michael, Machicao Fausto, Holzwarth Martin, Weisser Melanie, Maerker Elke, Teigeler Anna, Häring Hans, Fritsche Andreas

Abstract excerpt

Genetic factors play an important role in the pathogenesis of type 2 diabetes. The relevance to type 2 diabetes of the common polymorphism Glu23Lys in the potassium inward rectifier 6.2 (KIR6.2) gene is still controversial. The aim of this study was to assess whether this polymorphism influences beta-cell function, alpha-cell function, or insulin action. We therefore studied 298 nondiabetic subjects using an oral...

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Source

Identifiers

PMID: 12196481
DOI: 10.2337/diabetes.51.9.2854

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

The prevalent Glu23Lys polymorphism in the potassium inward rectifier 6.2 (KIR6.2) gene is associated with impaired glucagon suppression in response to hyperglycemia.PMID 12196481Read ↗

The E23K variant of Kir6.2 associates with impaired post-OGTT serum insulin response and increased risk of type 2 diabetes.Semantic proximity Read ↗

Variations in insulin secretion in carriers of the E23K variant in the KIR6.2 subunit of the ATP-sensitive K(+) channel in the beta-cell.Semantic proximity Read ↗

Current status of the E23K Kir6.2 polymorphism: implications for type-2 diabetesSemantic proximity Read ↗

Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance.Semantic proximity Read ↗

Co-localisation of the Kir6.2/SUR1 channel complex with glucagon-like peptide-1 and glucose-dependent insulinotrophic polypeptide expression in human ileal cells and implications for glycaemic control in new onset type 1 diabetes.Semantic proximity Read ↗

Combined risk allele score of eight type 2 diabetes genes is associated with reduced first-phase glucose-stimulated insulin secretion during hyperglycemic clamps.Semantic proximity Read ↗

Association of the Kir6.2 E23K variant with reduced acute insulin response in African-Americans.Semantic proximity Read ↗

The common single nucleotide polymorphism E23K in K(IR)6.2 sensitizes pancreatic beta-cell ATP-sensitive potassium channels toward activation through nucleoside diphosphates.Semantic proximity Read ↗

K(IR)6.2 polymorphism predisposes to type 2 diabetes by inducing overactivity of pancreatic beta-cell ATP-sensitive K(+) channels.Semantic proximity Read ↗

Genome-wide association study of circulating levels of glucagon during an oral glucose tolerance test.Semantic proximity Read ↗

Association of Kir6.2 and INS VNTR variants with glucose homeostasis in young obese.Semantic proximity Read ↗

An E23K single nucleotide polymorphism in the islet ATP-sensitive potassium channel gene (Kir6.2) contributes as much to the risk of Type II diabetes in Caucasians as the PPARγ Pro12Ala variantSemantic proximity Read ↗

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