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Article

ABCC8 (SUR1) and KCNJ11 (KIR6.2) mutations in persistent hyperinsulinemic hypoglycemia of infancy and evaluation of different therapeutic measures.

Journal of pediatric endocrinology & metabolism : JPEM - 1 Jan 2000

Darendeliler Feyza, Fournet Jean-Christophe, Baş Firdevs, Junien Claudine, Gross Marie-Sylvie, Bundak Rüveyde, Saka Nurçin, Günöz Hülya

Abstract excerpt

Persistent hyperinsulinemic hypoglycemia of infancy (PHHI) can occur as a result of mutations in the subunits that form the ATP-sensitive potassium channel (K+ATP) in pancreatic beta-cells which play a major role in modulating insulin secretion from the beta-cells. Mutations have been shown in the genes for these subunits, namely for the plasma membrane sulfonylurea receptor (SUR1), ABCC8, and its associated...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hyperinsulinism

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Share to Potassium Channels

Share to Potassium Channels, Inwardly Rectifying

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Source

Identifiers

PMID: 12199344
DOI: 10.1515/jpem.2002.15.7.993

Genes

ABCC8
KCNJ11

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.

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ABCC8 (SUR1) and KCNJ11 (KIR6.2) mutations in persistent hyperinsulinemic hypoglycemia of infancy and evaluation of different therapeutic measures.PMID 12199344Read ↗

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Characterization of genes encoding the pancreatic beta-cell ATP-sensitive K+ channel in persistent hyperinsulinemic hypoglycemia of infancy in Japanese patients.Semantic proximity Read ↗

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Update of mutations in the genes encoding the pancreatic beta-cell K(ATP) channel subunits Kir6.2 (KCNJ11) and sulfonylurea receptor 1 (ABCC8) in diabetes mellitus and hyperinsulinism.Semantic proximity Read ↗

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