ArticleDiabetes2013
A mouse model of human hyperinsulinism produced by the E1506K mutation in the sulphonylurea receptor SUR1.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Clinical and Genetic Characteristics ofJournal of diabetes research · 2021Pooled it
- Modelling the effects of human SUR1 R1420H variation on insulin secretory function using isogenic iPSC-derived pancreatic islets.Diabetologia · 2026Article
- Loss of Beta-Cell Identity and Function as a Mechanism of Secondary Failure of Sulfonylurea Therapy in Diabetes.MedComm · 2026Article
- Paradoxical Maturity-Onset Diabetes of the Young Arising From Loss-of-Function Mutations in ATP-Sensitive Potassium Channels.Diabetes · 2026Article
- VDAC1 is a target for pharmacologically induced insulin hypersecretion in β cells.Cell reports · 2025Article
- Beyond Redox Regulation: Novel Roles of TXNIP in the Pathogenesis and Therapeutic Targeting of Kidney Disease.The American journal of pathology · 2025Review
- A loss-of-function mutation in KCNJ11 causing sulfonylurea-sensitive diabetes in early adult life.Diabetologia · 2024Article
- Personalized Therapeutics for KAnnual review of pharmacology and toxicology · 2023Review
- Genome-edited zebrafish model ofIslets · 2022Article
- ATP-Sensitive Potassium Channels in Hyperinsulinism and Type 2 Diabetes: Inconvenient Paradox or New Paradigm?Diabetes · 2022Review
- SUR1-E1506K mutation impairs glucose tolerance and promotes vulnerable atherosclerotic plaque phenotype in hypercholesterolemic mice.PloS one · 2021Article
- Update of variants identified in the pancreatic β-cell KHuman mutation · 2020Review
- Identification of a compound heterozygous inactivating ABCC8 gene mutation responsible for young-onset diabetes with exome sequencing.Journal of diabetes investigation · 2020Article
- Pulmonary Hypertension and ATP-Sensitive Potassium Channels.Hypertension (Dallas, Tex. : 1979) · 2019Review
- Modulation of SUR1 KInternational journal of molecular sciences · 2019Article
- aThe characteristics of glucose metabolism in the sulfonylurea receptor 1 knockout rat model.Molecular medicine (Cambridge, Mass.) · 2019Article
- Article
- Absence of cannabinoid 1 receptor in beta cells protects against high-fat/high-sugar diet-induced beta cell dysfunction and inflammation in murine islets.Diabetologia · 2018Article
- Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.Physiological reviews · 2018Review
- KInternal medicine (Tokyo, Japan) · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Loss-of-function mutations in the KATP channel genes KCNJ11 and ABCC8 cause neonatal hyperinsulinism in humans. Dominantly inherited mutations cause less severe disease, which may progress to glucose intolerance and diabetes in later life (e.g., SUR1-E1506K). We generated a mouse expressing SUR1-E1506K in place of SUR1. KATP channel inhibition by MgATP was enhanced in both homozygous (homE1506K) and heterozygous (hetE1506K) mutant mice, due to impaired channel activation by MgADP. As a consequence, mutant β-cells showed less on-cell KATP channel activity and fired action potentials in glucose-free solution. HomE1506K mice exhibited enhanced insulin secretion and lower fasting blood glucose within 8 weeks of birth, but reduced insulin secretion and impaired glucose tolerance at 6 months of age. These changes correlated with a lower insulin content; unlike wild-type or hetE1506K mice, insulin content did not increase with age in homE1506K mice. There was no difference in the number and size of islets or β-cells in the three types of mice, or evidence of β-cell proliferation. We conclude that the gradual development of glucose intolerance in patients with the SUR1-E1506K mutation might, as in the mouse model, result from impaired insulin secretion due a failure of insulin content to increase with age.
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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.