ArticleDiabetes2001
Dysregulation of insulin secretion in children with congenital hyperinsulinism due to sulfonylurea receptor mutations.
Article in Diabetes, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
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Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 130 citations in OpenAlex.
- International Guidelines for the Diagnosis and Management of Hyperinsulinism.Hormone research in paediatrics · 2024Guideline
- Pharmacogenetics of glucose-lowering drug treatment: a systematic review.Molecular diagnosis & therapy · 2007Pooled it
- Functional evaluation of pancreatic islets from patients with Beckwith-Wiedemann syndrome and congenital hyperinsulinism.The Journal of clinical endocrinology and metabolism · 2026Article
- A selective nonpeptide somatostatin receptor 5 agonist effectively decreases insulin secretion in hyperinsulinism.The Journal of biological chemistry · 2023Article
- Neonatal and early-onset diabetes in Ukraine: Atypical features and mortality.Diabetic medicine : a journal of the British Diabetic Association · 2023Article
- New approaches to screening and management of neonatal hypoglycemia based on improved understanding of the molecular mechanism of hypoglycemia.Frontiers in pediatrics · 2023Review
- Genome-edited zebrafish model ofIslets · 2022Article
- Decreased KATP Channel Activity Contributes to the Low Glucose Threshold for Insulin Secretion of Rat Neonatal Islets.Endocrinology · 2021Article
- Novel dominant KAmerican journal of medical genetics. Part A · 2019Article
- Surgical treatment of congenital hyperinsulinism: Results from 500 pancreatectomies in neonates and children.Journal of pediatric surgery · 2019Article
- Nutrient sensing in pancreatic islets: lessons from congenital hyperinsulinism and monogenic diabetes.Annals of the New York Academy of Sciences · 2018Review
- Functional and Metabolomic Consequences of KDiabetes · 2017Article
- Uncovering the molecular pathogenesis of congenital hyperinsulinism by panel gene sequencing in 32 Chinese patients.Molecular genetics & genomic medicine · 2015Article
- Re-evaluating "transitional neonatal hypoglycemia": mechanism and implications for management.The Journal of pediatrics · 2015Review
- Uncoupling of secretion from growth in some hormone secretory tissues.The Journal of clinical endocrinology and metabolism · 2014Review
- Glucose-stimulated insulin secretion: A newer perspective.Journal of diabetes investigation · 2013Review
- The diabetic β-cell: hyperstimulated vs. hyperexcited.Diabetes, obesity & metabolism · 2012Review
- Nateglinide is Effective for Diabetes Mellitus with Reactive Hypoglycemia in a Child with a Compound Heterozygous ABCC8 Mutation.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2012Article
- Persistent hyperinsulinemic hypoglycemia of infancy: An overview of current concepts.Journal of Indian Association of Pediatric Surgeons · 2012Article
- Lessons in human biology from a monogenic pancreatic β cell disease.The Journal of clinical investigation · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
Mutations in the high-affinity sulfonylurea receptor (SUR)-1 cause one of the severe recessively inherited diffuse forms of congenital hyperinsulinism or, when associated with loss of heterozygosity, focal adenomatosis. We hypothesized that SUR1 mutations would render the beta-cell insensitive to sulfonylureas and to glucose. Stimulated insulin responses were compared among eight patients with diffuse hyperinsulinism (two mutations), six carrier parents, and ten normal adults. In the patients with diffuse hyperinsulinism, the acute insulin response to intravenous tolbutamide was absent and did not overlap with the responses seen in either adult group. There was positive, albeit significantly blunted, acute insulin response to intravenous dextrose in the patients with diffuse hyperinsulinism. Graded infusions of glucose, to raise and then lower plasma glucose concentrations over 4 h, caused similar rises in blood glucose but lower peak insulin levels in the hyperinsulinemic patients. Loss of acute insulin response to tolbutamide can identify children with diffuse SUR1 defects. The greater response to glucose than to tolbutamide indicates that ATP-sensitive potassium (KATP) channel-independent pathways are involved in glucose-mediated insulin release in patients with diffuse SUR1 defects. The diminished glucose responsiveness suggests that SUR1 mutations and lack of KATP channel activity may contribute to the late development of diabetes in patients with hyperinsulinism independently of subtotal pancreatectomy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.