Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Congenital hyperinsulinism caused by hexokinase I expression or glucokinase-activating mutation in a subset of β-cells.

Diabetes - 1 May 2013

Henquin Jean-Claude, Sempoux Christine, Marchandise Joelle, Godecharles Sebastien, Guiot Yves, Nenquin Myriam, Rahier Jacques

Abstract excerpt

Congenital hyperinsulinism causes persistent hypoglycemia in neonates and infants. Most often, uncontrolled insulin secretion (IS) results from a lack of functional K(ATP) channels in all β-cells or only in β-cells within a resectable focal lesion. In more rare cases, without K(ATP) channel mutations, hyperfunctional islets are confined within few lobules, whereas hypofunctional islets are present throughout the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Diazoxide
Share to Glucokinase

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hexokinase

Share to Hyperinsulinism

Share to Hypoglycemic Agents

Share to Insulin

Share to Insulin-Secreting Cells

Share to Insulin Secretion

Source

Open in PubMed Open full text

Identifiers

PMID: 23274908
DOI: 10.2337/db12-1414
PMCID: PMC3636634

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Congenital hyperinsulinism caused by hexokinase I expression or glucokinase-activating mutation in a subset of β-cells.PMID 23274908Read ↗

In vitro insulin secretion by pancreatic tissue from infants with diazoxide-resistant congenital hyperinsulinism deviates from model predictions.Semantic proximity Read ↗

Morphological mosaicism of the pancreatic islets: a novel anatomopathological form of persistent hyperinsulinemic hypoglycemia of infancy.Semantic proximity Read ↗

The focal form of persistent hyperinsulinemic hypoglycemia of infancy: morphological and molecular studies show structural and functional differences with insulinoma.Semantic proximity Read ↗

Phenotypic Characterization of Congenital Hyperinsulinism Due to Novel Activating Glucokinase Mutations.Semantic proximity Read ↗

Nutrient sensing in pancreatic islets: lessons from congenital hyperinsulinism and monogenic diabetes.Semantic proximity Read ↗

The difficult management of persistent, non-focal congenital hyperinsulinism: A retrospective review from a single, tertiary center.Semantic proximity Read ↗

Hyperinsulinism of the newborn.Semantic proximity Read ↗

Focal congenital hyperinsulinism managed by medical treatment: a diagnostic algorithm based on molecular genetic screening.Semantic proximity Read ↗

Hyperinsulinemic hypoglycemia of infancy: the challenge continues.Semantic proximity Read ↗

A multidisciplinary approach to the focal form of congenital hyperinsulinism leads to successful treatment by partial pancreatectomy.Semantic proximity Read ↗

KATP channel mutations in congenital hyperinsulinism: Progress and challenges towards mechanism-based therapies.Semantic proximity Read ↗

Targeted overactivity of beta cell K(ATP) channels induces profound neonatal diabetes.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.