ArticleCell metabolism2011
Control of pancreatic β cell regeneration by glucose metabolism.
Article in Cell metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers, 2 of them syntheses that pooled it.
What it found
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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
206 citing papers in PubMed, 2 syntheses or guidelines pooled it, 300 citations in OpenAlex.
- Efficacy of mesenchymal stem cell therapy on glucose levels in type 2 diabetes mellitus: A systematic review and meta-analysis.Journal of diabetes investigation · 2021Pooled it
- Insulin gene mutations and posttranslational and translocation defects: associations with diabetes.Endocrine · 2020Pooled it
- Trial
- Postnatal refinement of CaChannels (Austin, Tex.) · 2026Article
- Metabolic Programming of β-Cell Fate, State, and Function through Time and Space.Physiology (Bethesda, Md.) · 2026Review
- ChREBP drives β-cell proliferation under metabolic stress but not in pregnancy-induced β-cell expansion.Journal of diabetes investigation · 2026Article
- Redefining β-Cell Function in Type 2 Diabetes Mellitus: From Comprehensive Assessment to Precision Medicine.Diabetes & metabolism journal · 2026Review
- Endothelial IRE1α promotes thrombospondin-1 mRNA decay and supports metabolic stress adaptation of pancreatic islets.Nature communications · 2026Article
- The protein deacetylase SIRT2 exerts metabolic control over adaptive β cell proliferation.The Journal of clinical investigation · 2025Article
- Drug-induced regeneration of pancreatic beta cells: An approach to cellular therapeutic targets.Cell regeneration (London, England) · 2025Review
- Renalase inhibition defends against acute and chronic β cell stress by regulating cell metabolism.Molecular metabolism · 2025Article
- Betagenin ameliorates diabetes by inducing insulin secretion and β-cell proliferation.The Journal of biological chemistry · 2025Article
- Evolving Characteristics of Type 2 Diabetes Mellitus in East Asia.Endocrinology and metabolism (Seoul, Korea) · 2025Review
- Interactions between islet-resident macrophages and β cells in diabetes.Frontiers in immunology · 2025Review
- Harnessing beta-cell replication: advancing molecular insights to regenerative therapies in diabetes.Frontiers in endocrinology · 2025Review
- Effects of glucokinase haploinsufficiency on the pancreatic β-cell mass and function of long-term high-fat, high-sucrose diet-fed mice.Journal of diabetes investigation · 2024Article
- Glucokinase (GCK) in diabetes: from molecular mechanisms to disease pathogenesis.Cellular & molecular biology letters · 2024Review
- ANS-SCMC: A matrix completion method based on adaptive neighbourhood similarity and sparse constraints for predicting microbe-disease associations.Journal of cellular and molecular medicine · 2024Article
- Dual role of neuroplastin in pancreatic β cells: Regulating insulin secretion and promoting islet inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Moderate beta-cell ablation triggers synergic compensatory mechanisms even in the absence of overt metabolic disruption.Communications biology · 2024Article
146 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
Abstract
Recent studies revealed a surprising regenerative capacity of insulin-producing β cells in mice, suggesting that regenerative therapy for human diabetes could in principle be achieved. Physiologic β cell regeneration under stressed conditions relies on accelerated proliferation of surviving β cells, but the factors that trigger and control this response remain unclear. Using islet transplantation experiments, we show that β cell mass is controlled systemically rather than by local factors such as tissue damage. Chronic changes in β cell glucose metabolism, rather than blood glucose levels per se, are the main positive regulator of basal and compensatory β cell proliferation in vivo. Intracellularly, genetic and pharmacologic manipulations reveal that glucose induces β cell replication via metabolism by glucokinase, the first step of glycolysis, followed by closure of K(ATP) channels and membrane depolarization. Our data provide a molecular mechanism for homeostatic control of β cell mass by metabolic demand.
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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.