ArticleScientific reports2017
Modeling Congenital Hyperinsulinism with ABCC8-Deficient Human Embryonic Stem Cells Generated by CRISPR/Cas9.
Article in Scientific reports, 2017. 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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14 citing papers in PubMed, 21 citations in OpenAlex.
- Patient-derived induced pluripotent stem cells for precision modelling of monogenic beta cell disorders.Frontiers in endocrinology · 2026Review
- Integrative single-cell multi-omics profiling of human pancreatic islets identifies T1D-associated genes and regulatory signals.Cell reports · 2025Article
- Biomedical applications of organoids in genetic diseases.Medical review (2021) · 2025Review
- Review
- Islet organoid as a promising model for diabetes.Protein & cell · 2022Review
- Heterogeneous network propagation with forward similarity integration to enhance drug-target association prediction.PeerJ. Computer science · 2022Article
- Stem Cell Based Models in Congenital Hyperinsulinism - Perspective on Practicalities and Possibilities.Frontiers in endocrinology · 2022Review
- SUR1-mutant iPS cell-derived islets recapitulate the pathophysiology of congenital hyperinsulinism.Diabetologia · 2021Article
- Human Pluripotent Stem Cells Go Diabetic: A Glimpse on Monogenic Variants.Frontiers in endocrinology · 2021Review
- Human Pluripotent Stem Cells to Model Islet Defects in Diabetes.Frontiers in endocrinology · 2021Review
- Article
- Human Pluripotent Stem Cells: A Unique Tool for Toxicity Testing in Pancreatic Progenitor and Endocrine Cells.Frontiers in endocrinology · 2020Article
- Somatostatin analogues for the treatment of hyperinsulinaemic hypoglycaemia.Therapeutic advances in endocrinology and metabolism · 2020Review
- Concise Review: Human Pluripotent Stem Cells for the Modeling of Pancreatic β-Cell Pathology.Stem cells (Dayton, Ohio) · 2019Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Congenital hyperinsulinism (CHI) is a rare genetic disorder characterized by excess insulin secretion, which results in hypoglycemia. Mutation of sulfonylurea receptor 1 (SUR1), encoded by the ABCC8 gene, is the main cause of CHI. Here, we captured the phenotype of excess insulin secretion through pancreatic differentiation of ABCC8-deficient stem cells generated by the CRISPR/Cas9 system. ABCC8-deficient insulin-producing cells secreted higher insulin than their wild-type counterparts, and the excess insulin secretion was rescued by nifedipine, octreotide and nicorandil. Further, we tested the role of SUR1 in response to different potassium levels and found that dysfunction of SUR1 decreased the insulin secretion rate in low and high potassium environments. Hence, pancreatic differentiation of ABCC8-deficient cells recapitulated the CHI disease phenotype in vitro, which represents an attractive model to further elucidate the function of SUR1 and to develop and screen for novel therapeutic drugs.
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