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

Hyperinsulinism of infancy: the regulated release of insulin by KATP channel-independent pathways.

Diabetes - 1 Feb 2001

Straub S G, Cosgrove K E, Ammälä C, Shepherd R M, O'Brien R E, Barnes P D, Kuchinski N, Chapman J C, Schaeppi M, Glaser B, Lindley K J, Sharp G W, Aynsley-Green A, Dunne M J

Abstract excerpt

Hyperinsulinism of infancy (HI) is a congenital defect in the regulated release of insulin from pancreatic beta-cells. Here we describe stimulus-secretion coupling mechanisms in beta-cells and intact islets of Langerhans isolated from three patients with a novel SUR1 gene defect. 2154+3 A to G SU...

Read the complete abstract on PubMed

Topics

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

Share to Adenosine Diphosphate
Share to Exocytosis
Share to Hyperinsulinism

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Insulin Secretion

Share to Islets of Langerhans

Share to Potassium Channels, Inwardly Rectifying

Share to Receptors, Drug

Share to Sulfonylurea Receptors

Source

Identifiers

PMID: 11272144
DOI: 10.2337/diabetes.50.2.329

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-11272144-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

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

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Hyperinsulinism of infancy: the regulated release of insulin by KATP channel-independent pathways.PMID 11272144Read ↗

K(ATP) channels and insulin secretion disorders.Semantic proximity Read ↗

Sur1 Knockout MiceSemantic proximity Read ↗

Hyperinsulinism in Infancy: From Basic Science to Clinical DiseaseSemantic proximity Read ↗

Familial hyperinsulinism and pancreatic beta-cell ATP-sensitive potassium channels.Semantic proximity Read ↗

Hyperinsulinism in infancy: understanding the pathophysiology.Semantic proximity Read ↗

ATP-Sensitive Potassium Channels in Hyperinsulinism and Type 2 Diabetes: Inconvenient Paradox or New Paradigm?Semantic proximity Read ↗

A rare mutation in ABCC8/SUR1 leading to altered ATP-sensitive K+ channel activity and beta-cell glucose sensing is associated with type 2 diabetes in adults.Semantic proximity Read ↗

Sulfonylurea receptor type 1 knock-out mice have intact feeding-stimulated insulin secretion despite marked impairment in their response to glucose.Semantic proximity Read ↗

Congenital hyperinsulinism: molecular basis of a heterogeneous disease.Semantic proximity Read ↗

The role of ATP sensitive channels in insulin secretion and the implications in persistent hyperinsulinemic hypoglycaemia of infancy (PHHI).Semantic proximity Read ↗

Identification and Rescue of Congenital Hyperinsulinism-Associated <i>ABCC8</i> Mutations that Impair K <sub>ATP</sub> Channel TraffickingSemantic proximity Read ↗

Hyperinsulinemic hypoglycemia of infancy. Recent insights into ATP-sensitive potassium channels, sulfonylurea receptors, molecular mechanisms, and treatment.Semantic proximity Read ↗

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