ArticleDiabetes2015
Altered Phenotype of β-Cells and Other Pancreatic Cell Lineages in Patients With Diffuse Congenital Hyperinsulinism in Infancy Caused by Mutations in the ATP-Sensitive K-Channel.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Modelling the effects of human SUR1 R1420H variation on insulin secretory function using isogenic iPSC-derived pancreatic islets.Diabetologia · 2026Article
- Cells Co-Producing Insulin and Glucagon in Congenital Hyperinsulinism.Life (Basel, Switzerland) · 2025Article
- Chromosome 20p11.2 deletions cause congenital hyperinsulinism via the loss of FOXA2 or its regulatory elements.European journal of human genetics : EJHG · 2024Article
- The Human Islet: Mini-Organ With Mega-Impact.Endocrine reviews · 2021Review
- SUR1-mutant iPS cell-derived islets recapitulate the pathophysiology of congenital hyperinsulinism.Diabetologia · 2021Article
- Animal Models of Pancreas Development, Developmental Disorders, and Disease.Advances in experimental medicine and biology · 2020Review
- Article
- Ablation of somatostatin cells leads to impaired pancreatic islet function and neonatal death in rodents.Cell death & disease · 2018Article
- Clinical Diversity in Focal Congenital Hyperinsulinism in Infancy Correlates With Histological Heterogeneity of Islet Cell Lesions.Frontiers in endocrinology · 2018Article
- Atypical Forms of Congenital Hyperinsulinism in Infancy Are Associated With Mosaic Patterns of Immature Islet Cells.The Journal of clinical endocrinology and metabolism · 2017Article
- Hyperinsulinemic hypoglycemia: clinical, molecular and therapeutical novelties.Journal of inherited metabolic disease · 2017Review
- Let-7e modulates the inflammatory response in vascular endothelial cells through ceRNA crosstalk.Scientific reports · 2017Article
- Enhanced Islet Cell Nucleomegaly Defines Diffuse Congenital Hyperinsulinism in Infancy but Not Other Forms of the Disease.American journal of clinical pathology · 2016Article
- Genome-edited human stem cell-derived beta cells: a powerful tool for drilling down on type 2 diabetes GWAS biology.F1000Research · 2016Review
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Diffuse congenital hyperinsulinism in infancy (CHI-D) arises from mutations inactivating the KATP channel; however, the phenotype is difficult to explain from electrophysiology alone. Here we studied wider abnormalities in the β-cell and other pancreatic lineages. Islets were disorganized in CHI-D compared with controls. PAX4 and ARX expression was decreased. A tendency toward increased NKX2.2 expression was consistent with its detection in two-thirds of CHI-D δ-cell nuclei, similar to the fetal pancreas, and implied immature δ-cell function. CHI-D δ-cells also comprised 10% of cells displaying nucleomegaly. In CHI-D, increased proliferation was most elevated in duct (5- to 11-fold) and acinar (7- to 47-fold) lineages. Increased β-cell proliferation observed in some cases was offset by an increase in apoptosis; this is in keeping with no difference in INSULIN expression or surface area stained for insulin between CHI-D and control pancreas. However, nuclear localization of CDK6 and P27 was markedly enhanced in CHI-D β-cells compared with cytoplasmic localization in control cells. These combined data support normal β-cell mass in CHI-D, but with G1/S molecules positioned in favor of cell cycle progression. New molecular abnormalities in δ-cells and marked proliferative increases in other pancreatic lineages indicate CHI-D is not solely a β-cell disorder.
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Registered trials
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