ArticleCell metabolism2014
Pancreatic β cell dedifferentiation in diabetes and redifferentiation following insulin therapy.
Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 260 papers.
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Who cites it
260 citing papers in PubMed, 405 citations in OpenAlex.
- Intense simplified strategy for newly diagnosed type 2 diabetes in patients with severe hyperglycaemia: multicentre, open label, randomised trial.BMJ (Clinical research ed.) · 2024Trial
- Body weight and metabolic risk factors in patients with type 2 diabetes on a self-selected high-protein low-carbohydrate diet.European journal of nutrition · 2021Trial
- Exenatide, Metformin, or Both for Prediabetes in PCOS: A Randomized, Open-label, Parallel-group Controlled Study.The Journal of clinical endocrinology and metabolism · 2021Trial
- Transcription factor 7-like 2 gene links increased in vivo insulin synthesis to type 2 diabetes.EBioMedicine · 2018Trial
- BAF60A governs beta cell identity to control systemic glucose homeostasis.Diabetologia · 2026Article
- Effects of MCC950 on lipid profiles, glycemic control, and sympathetic dysfunction in a streptozotocin-induced type 1 diabetic rat model.Croatian medical journal · 2026Article
- Syntaxin-4, a key exocytosis mediating protein, shows heterogeneous expression in insulin-positive cells of human donors with new-onset and longer duration of type 1 diabetes: comparison with non-diabetic autoantibody-positive and -negative donors.Journal of molecular histology · 2026Article
- SOX9: dosage- and context-dependent functions in pancreatic development and β-cell biology.Cell communication and signaling : CCS · 2026Review
- Zinc accumulation-induced integrated stress response triggers β-cell identity loss.Cell research · 2026Article
- Investigational treatments of β-cell failure and replacement.Diabetology international · 2026Review
- Mitochondria as Epigenetic Regulators of β-Cell Identity and Plasticity: A Metabolo-Epigenetic Perspective.Cells · 2026Review
- LDHA induces beta cell dedifferentiation in diabetes through metabolic and epigenetic reprogramming.Diabetologia · 2026Article
- Artificial intelligence-based comparison of the effects of duodenojejunostomy and sleeve gastrectomy on pancreatic morphology in Zucker diabetic fatty rats.Frontiers in surgery · 2026Article
- Cells Co-Producing Insulin and Glucagon in Congenital Hyperinsulinism.Life (Basel, Switzerland) · 2025Article
- Western Diet Induces Changes in Gene Expression in Multiple Tissues During Early Insulin Resistance and Glucose Intolerance in Male C57BL/6 Mice.Current issues in molecular biology · 2025Article
- Restoration of pancreatic beta cell identity and autophagy in KDiabetologia · 2025Article
- Article
- β-cell dedifferentiation in type 2 diabetes: Interplay of metabolic stress, endoplasmic reticulum dysfunction, and forkhead box protein O1 inhibition.World journal of diabetes · 2025Article
- March5-mediated Trim28 degradation preserves islet β-cell function in mice.Nature communications · 2025Article
- Partial remission of type 1 diabetes: Do immunometabolic events define the honeymoon period?Diabetes, obesity & metabolism · 2025Review
200 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes is characterized by "glucotoxic" loss of pancreatic β cell function and insulin content, but underlying mechanisms remain unclear. A mouse model of insulin-secretory deficiency induced by β cell inexcitability (K(ATP) gain of function) demonstrates development of diabetes and reiterates the features of human neonatal diabetes. In the diabetic state, β cells lose their mature identity and dedifferentiate to neurogenin3-positive and insulin-negative cells. Lineage-tracing experiments show that dedifferentiated cells can subsequently redifferentiate to mature neurogenin3-negative, insulin-positive β cells after lowering of blood glucose by insulin therapy. We demonstrate here that β cell dedifferentiation, rather than apoptosis, is the main mechanism of loss of insulin-positive cells, and redifferentiation accounts for restoration of insulin content and antidiabetic drug responsivity in these animals. These results may help explain gradual decrease in β cell mass in long-standing diabetes and recovery of β cell function and drug responsivity in type 2 diabetic patients following insulin therapy, and they suggest an approach to rescuing "exhausted" β cells in diabetes.
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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.