ArticleAmerican journal of physiology. Endocrinology and metabolism2014
Overnutrition induces β-cell differentiation through prolonged activation of β-cells in zebrafish larvae.
Article in American journal of physiology. Endocrinology and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Effects of overfeeding and high-fat diet on cardiosomatic parameters and cardiac structures in young and adult zebrafish.Fish physiology and biochemistry · 2017Trial
- tBid-Mediated Genetic Ablation of Connective Tissue Cells Reveals Their Key Regulatory Function During Limb Regeneration in Axolotls.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ppid is necessary for overnutrition-induced β-cell loss.American journal of physiology. Endocrinology and metabolism · 2026Article
- Mosloflavone induces pancreatic α cells transdifferentiation into β cells through PDX1.Journal of natural medicines · 2026Article
- Zebrafish as an effective model for accelerating diabetes research from discovery to therapy.Journal of diabetes and metabolic disorders · 2025Review
- Multifunctional Fluorescent Probe for Simultaneous Detection of ATP, Cys, Hcy, and GSH: Advancing Insights into Epilepsy and Liver Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Kinesin-1 mediates proper ER folding of the CaEMBO reports · 2024Article
- Hinokione: an abietene diterpene with pancreatic β cells regeneration and hypoglycemic activity, and other derivatives with novel structures from the woods of Agathis dammara.Journal of natural medicines · 2024Article
- Compounds from Agathis dammara exert hypoglycaemic activity by enhancing glucose uptake: lignans, terpenes and others.Natural products and bioprospecting · 2024Article
- Animal Models for Understanding the Mechanisms of Beta Cell Death during Type 2 Diabetes Pathogenesis.Biomedicines · 2024Review
- A New Hypoglycemic Prenylated Indole AlkaloidInternational journal of molecular sciences · 2023Article
- Research Progress on the Construction and Application of a Diabetic Zebrafish Model.International journal of molecular sciences · 2023Review
- Epigenetic modulation of cell fate during pancreas development.Trends in developmental biology · 2023Article
- Brasilterpenes A-E, Bergamotane Sesquiterpenoid Derivatives with Hypoglycemic Activity from the Deep Sea-Derived FungusMarine drugs · 2022Article
- RIPK3-mediated inflammation is a conserved β cell response to ER stress.Science advances · 2020Article
- In vivo generation and regeneration of β cells in zebrafish.Cell regeneration (London, England) · 2020Review
- Genomic knockout of alms1 in zebrafish recapitulates Alström syndrome and provides insight into metabolic phenotypes.Human molecular genetics · 2019Article
- Beta-cell excitability and excitability-driven diabetes in adult Zebrafish islets.Physiological reports · 2019Article
- Optimizing the Use of Zebrafish Feeding Trials for the Safety Evaluation of Genetically Modified Crops.International journal of molecular sciences · 2019Article
- Vegfa/vegfr2 signaling is necessary for zebrafish islet vessel development, but is dispensable for beta-cell and alpha-cell formation.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Insulin from islet β-cells maintains glucose homeostasis by stimulating peripheral tissues to remove glucose from circulation. Persistent elevation of insulin demand increases β-cell number through self-replication or differentiation (neogenesis) as part of a compensatory response. However, it is not well understood how a persistent increase in insulin demand is detected. We have previously demonstrated that a persistent increase in insulin demand by overnutrition induces compensatory β-cell differentiation in zebrafish. Here, we use a series of pharmacological and genetic analyses to show that prolonged stimulation of existing β-cells is necessary and sufficient for this compensatory response. In the absence of feeding, tonic, but not intermittent, pharmacological activation of β-cell secretion was sufficient to induce β-cell differentiation. Conversely, drugs that block β-cell secretion, including an ATP-sensitive potassium (K ATP) channel agonist and an L-type Ca(2+) channel blocker, suppressed overnutrition-induced β-cell differentiation. Genetic experiments specifically targeting β-cells confirm existing β-cells as the overnutrition sensor. First, inducible expression of a constitutively active K ATP channel in β-cells suppressed the overnutrition effect. Second, inducible expression of a dominant-negative K ATP mutant induced β-cell differentiation independent of nutrients. Third, sensitizing β-cell metabolism by transgenic expression of a hyperactive glucokinase potentiated differentiation. Finally, ablation of the existing β-cells abolished the differentiation response. Taken together, these data establish that overnutrition induces β-cell differentiation in larval zebrafish through prolonged activation of β-cells. These findings demonstrate an essential role for existing β-cells in sensing overnutrition and compensating for their own insufficiency by recruiting additional β-cells.
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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.