Evidence map›Paper›PMID 27398620›Full record

ArticleNature2016

Identification of proliferative and mature β-cells in the islets of Langerhans.

Erik Bader, Adriana Migliorini, Moritz Gegg, Noah Moruzzi, Jantje Gerdes, Sara S Roscioni, Mostafa Bakhti, Elisabeth Brandl, Martin Irmler, Johannes Beckers and 16 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers.

0numbers the graph read from it
0cells of the map it votes in
236citing papers in PubMed
40.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

236 citing papers in PubMed, 345 citations in OpenAlex.

  1. Postnatal refinement of CaChannels (Austin, Tex.) · 2026
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  14. Genetic recording of pancreatic beta cell proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  15. Article
  16. CD168 Identifies Proliferating Pancreatic Islet Cells in Murine and Human.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  17. Engineering hypoimmune stem cell-derived beta cells.Stem cell research & therapy · 2025
    Review
  18. Article
  19. Article
  20. Review

176 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

26 authors at 8 institutions in 2 countries.

Erik Bader
Adriana Migliorini
Moritz Gegg
Noah Moruzzi
Jantje Gerdes
Sara S Roscioni
Mostafa Bakhti
Elisabeth Brandl
Martin Irmler
Johannes Beckers
Michaela Aichler
Annette Feuchtinger
Christin Leitzinger
Hans Zischka
Rui Wang-Sattler
Martin Jastroch
Matthias Tschöp
Fausto Machicao
Harald Staiger
Hans-Ulrich Häring
Helena Chmelova
Julie A Chouinard
Nikolay Oskolkov
Olle Korsgren
Stephan Speier
Heiko Lickert
Helmholtz Zentrum München · DEHeinrich Heine University Düsseldorf · DEDeutsches Diabetes-Zentrum e.V. · DEKarolinska University Hospital · SELund University · SEPaul Langerhans Institute Dresden · DETechnical University of Munich · DEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin-dependent diabetes is a complex multifactorial disorder characterized by loss or dysfunction of β-cells. Pancreatic β-cells differ in size, glucose responsiveness, insulin secretion and precursor cell potential; understanding the mechanisms that underlie this functional heterogeneity might make it possible to develop new regenerative approaches. Here we show that Fltp (also known as Flattop and Cfap126), a Wnt/planar cell polarity (PCP) effector and reporter gene acts as a marker gene that subdivides endocrine cells into two subpopulations and distinguishes proliferation-competent from mature β-cells with distinct molecular, physiological and ultrastructural features. Genetic lineage tracing revealed that endocrine subpopulations from Fltp-negative and -positive lineages react differently to physiological and pathological changes. The expression of Fltp increases when endocrine cells cluster together to form polarized and mature 3D islet mini-organs. We show that 3D architecture and Wnt/PCP ligands are sufficient to trigger β-cell maturation. By contrast, the Wnt/PCP effector Fltp is not necessary for β-cell development, proliferation or maturation. We conclude that 3D architecture and Wnt/PCP signalling underlie functional β-cell heterogeneity and induce β-cell maturation. The identification of Fltp as a marker for endocrine subpopulations sheds light on the molecular underpinnings of islet cell heterogeneity and plasticity and might enable targeting of endocrine subpopulations for the regeneration of functional β-cell mass in diabetic patients.

Indexed as

AnimalsBiomarkersCell DifferentiationCell LineageCell PolarityCell ProliferationHumansInsulin ResistanceIslets of LangerhansLigandsMiceMice, Inbred C57BLMicrotubule-Associated ProteinsWnt Signaling PathwayBiomarkersFlattop protein, mouseLigandsMicrotubule-Associated Proteins

Identifiers

PMID27398620
OpenAlexW2465180814

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.