ArticleDiabetologia2016
Extreme obesity induces massive beta cell expansion in mice through self-renewal and does not alter the beta cell lineage.
Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development.Nature communications · 2026Article
- Islet single-cell transcriptomic profiling during obesity-induced beta cell expansion in female mice.iScience · 2025Article
- Moderate beta-cell ablation triggers synergic compensatory mechanisms even in the absence of overt metabolic disruption.Communications biology · 2024Article
- β-Cell Regeneration Is Driven by Pancreatic Plasticity.Advances in anatomy, embryology, and cell biology · 2024Review
- Cell identity dynamics and insight into insulin secretagogues when employing stem cell-derived islets for disease modeling.Frontiers in bioengineering and biotechnology · 2024Article
- Matters arising: Insufficient evidence that pancreatic β cells are derived from adult ductal Neurog3-expressing progenitors.Cell stem cell · 2023Article
- The rheumatoid arthritis drug auranofin lowers leptin levels and exerts antidiabetic effects in obese mice.Cell metabolism · 2022Article
- Txnip deficiency promotes β-cell proliferation in the HFD-induced obesity mouse model.Endocrine connections · 2022Article
- Spata7 is required for maintenance of the retinal connecting cilium.Scientific reports · 2022Article
- Decreased proliferation of aged rat beta cells corresponds with enhanced expression of the cell cycle inhibitor p27Biology of the cell · 2021Article
- Stem/progenitor cells in normal physiology and disease of the pancreas.Molecular and cellular endocrinology · 2021Review
- Restoring normal islet mass and function in type 1 diabetes through regenerative medicine and tissue engineering.The lancet. Diabetes & endocrinology · 2021Review
- Probing β-Cell Biology in Space and Time.Diabetes · 2021Review
- Pancreatic β cell regeneration: To β or not to β.Current opinion in physiology · 2020Article
- Toll-like receptors TLR2 and TLR4 block the replication of pancreatic β cells in diet-induced obesity.Nature immunology · 2019Article
- Glucagon Receptor Antagonist-Stimulated α-Cell Proliferation Is Severely Restricted With Advanced Age.Diabetes · 2019Article
- Friendly Fat Theory - Explaining the Paradox of Diabetes and Obesity.European endocrinology · 2019Review
- Article
- Evidence for a Neogenic Niche at the Periphery of Pancreatic Islets.BioEssays : news and reviews in molecular, cellular and developmental biology · 2018Review
- (Re)generating Human Beta Cells: Status, Pitfalls, and Perspectives.Physiological reviews · 2018Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
aims/hypothesisUnderstanding the developmental biology of beta cell regeneration is critical for developing new diabetes therapies. Obesity is a potent but poorly understood stimulus for beta cell expansion. Current models of obesity are complicated by developmental compensation or concurrent diabetes, limiting their usefulness for identifying the lineage mechanism(s) of beta cell expansion. We aimed to determine whether acute inducible obesity stimulates beta cell expansion and to determine the lineage mechanism of beta cell growth in obesity.
methodsWe created whole-body tamoxifen-inducible leptin receptor (LepR)-deficient mice (Ubc-Cre (ERT2) LepR (loxP/loxP) ) as a novel model of acute obesity. Beta cell mass and proliferation were quantified after short-term LepR deletion. Clonal analysis of beta cell expansion using the Brainbow2.1 reporter was performed 6 months post tamoxifen initiation.
resultsLepR deficiency induced a doubling of body mass within 3 weeks, with moderate glucose intolerance (unlike typical LepR mutant mice [db/db], which have frank diabetes). Beta cell mass expanded threefold through increased beta cell proliferation, without evidence for contribution from specialised progenitors or stem cells (via sequential thymidine labelling and Brainbow2.1 reporter). Thus, self-renewal is the primary lineage mechanism in obesity-induced beta cell expansion. However, even the rapid beta cell proliferation could not exceed the restrictions of the replication refractory period. CONCLUSIONS/
interpretationIn summary, we created a novel model of inducible obesity demonstrating that even extreme metabolic demand does not alter beta cell lineage.
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