ArticleDiabetes2012
Nutrient excess stimulates β-cell neogenesis in zebrafish.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- ZRANB3 is an African-specific type 2 diabetes locus associated with beta-cell mass and insulin response.Nature communications · 2019Pooled it
- 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
- HNF1α-Q125ter-mediated mitochondrial dysfunction and impaired mitophagy in β-cells.Journal of molecular endocrinology · 2025Article
- Functionally characterizing obesity-susceptibility genes using CRISPR/Cas9, in vivo imaging and deep learning.Scientific reports · 2025Article
- Examining the liver-pancreas crosstalk reveals a role for the molybdenum cofactor in β-cell regeneration.Life science alliance · 2024Article
- Maternal Western-style diet in nonhuman primates leads to offspring islet adaptations including altered gene expression and insulin hypersecretion.American journal of physiology. Endocrinology and metabolism · 2023Article
- Loss of RREB1 in pancreatic beta cells reduces cellular insulin content and affects endocrine cell gene expression.Diabetologia · 2023Article
- Protocol to evaluate hyperlipidemia in zebrafish larvae.STAR protocols · 2022Article
- Novel Loss-of-Function Variant in HNF1a Induces β-Cell Dysfunction through Endoplasmic Reticulum Stress.International journal of molecular sciences · 2022Article
- Macrophages and neutrophils are necessary for ER stress-induced β cell loss.Cell reports · 2022Article
- The Nrf2a pathway impacts zebrafish offspring development with maternal preconception exposure to perfluorobutanesulfonic acid.Chemosphere · 2022Article
- Knockout of Nur77 Leads to Amino Acid, Lipid, and Glucose Metabolism Disorders in Zebrafish.Frontiers in endocrinology · 2022Article
- Exocrine pancreas proteases regulate β-cell proliferation in zebrafish ciliopathy models and in murine systems.Biology open · 2021Article
- 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
- Article
- Primary Cilium, An Unsung Hero in Maintaining Functional β-cell Population.The Yale journal of biology and medicine · 2019Review
- Corosolic acid isolated from Eriobotrya japonica leaves reduces glucose level in human hepatocellular carcinoma cells, zebrafish and rats.Scientific reports · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Persistent nutrient excess results in a compensatory increase in the β-cell number in mammals. It is unknown whether this response occurs in nonmammalian vertebrates, including zebrafish, a model for genetics and chemical genetics. We investigated the response of zebrafish β-cells to nutrient excess and the underlying mechanisms by culturing transgenic zebrafish larvae in solutions of different nutrient composition. The number of β-cells rapidly increases after persistent, but not intermittent, exposure to glucose or a lipid-rich diet. The response to glucose, but not the lipid-rich diet, required mammalian target of rapamycin activity. In contrast, inhibition of insulin/IGF-1 signaling in β-cells blocked the response to the lipid-rich diet, but not to glucose. Lineage tracing and marker expression analyses indicated that the new β-cells were not from self-replication but arose through differentiation of postmitotic precursor cells. On the basis of transgenic markers, we identified two groups of newly formed β-cells: one with nkx2.2 promoter activity and the other with mnx1 promoter activity. Thus, nutrient excess in zebrafish induces a rapid increase in β-cells though differentiation of two subpopulations of postmitotic precursor cells. This occurs through different mechanisms depending on the nutrient type and likely involves paracrine signaling between the differentiated β-cells and the precursor 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.