Evidence map›Paper›PMID 23354125›Full record

ArticleDiabetologia2013

Molecular basis for the regulation of islet beta cell mass in mice: the role of E-cadherin.

N Wakae-Takada, S Xuan, K Watanabe, P Meda, R L Leibel

Open access · bronzeAbstract read
In one paragraph

Article in Diabetologia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
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  8. Review
  9. Article
  10. Is type 2 diabetes mellitus another intercellular junction-related disorder?Experimental biology and medicine (Maywood, N.J.) · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Pancreatic β-cell heterogeneity in health and diabetes: classes, sources, and subtypes.American journal of physiology. Endocrinology and metabolism · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

N Wakae-TakadaDepartment of Pediatrics, Columbia University, New York, NY, USA.
S Xuan
K Watanabe
P Meda
R L Leibel
Columbia University · USUniversity of Geneva · CH

Funding

Translational Biomarker Analytical Core (TBAC)P30DK063608 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI DOMENICO ACCILI · 2003 to 2026
$36.7M
RESEARCH TRAININGP30DK026687 · NIDDK · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS · PI Anthony W Ferrante, DYMPNA GALLAGHER · 1986 to 2026
$33.0M
Cloning of a type 2 diabetes modifier in obese miceR01DK066518 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LEIBEL, RUDOLPH L · 2003 to 2011
$4.2M
NIDDK NIH HHS 5P30DK63608NIDDK NIH HHS NIH DK66518NIDDK NIH HHS P30 DK026687NIDDK NIH HHS P30 DK063608NIDDK NIH HHS R01 DK066518
6 · The paper itself

Abstract

aims/hypothesisIn rodents and humans, the rate of beta cell proliferation declines rapidly after birth; formation of the islets of Langerhans begins perinatally and continues after birth. Here, we tested the hypothesis that increasing levels of E-cadherin during islet formation mediate the decline in beta cell proliferation rate by contributing to a reduction of nuclear β-catenin and D-cyclins.

methodsWe examined E-cadherin, nuclear β-catenin, and D-cyclin levels, as well as cell proliferation during in vitro and in vivo formation of islet cell aggregates, using β-TC6 cells and transgenic mice with green fluorescent protein (GFP)-labelled beta cells, respectively. We tested the role of E-cadherin using antisense-mediated reductions of E-cadherin in β-TC6 cells, and mice segregating for a beta cell-specific E-cadherin knockout (Ecad [also known as Cdh1] βKO).

resultsIn vitro, pseudo-islets of β-TC6 cells displayed increased E-cadherin but decreased nuclear β-catenin and cyclin D2, and reduced rates of cell proliferation, compared with monolayers. Antisense knockdown of E-cadherin increased cell proliferation and levels of cyclins D1 and D2. After birth, beta cells showed increased levels of E-cadherin, but decreased levels of D-cyclin, whereas islets of Ecad βKO mice showed increased levels of D-cyclins and nuclear β-catenin, as well as increased beta cell proliferation. These islets were significantly larger than those of control mice and displayed reduced levels of connexin 36. These changes correlated with reduced insulin response to ambient glucose, both in vitro and in vivo. CONCLUSIONS/

interpretationThe findings support our hypothesis by indicating an important role of E-cadherin in the control of beta cell mass and function.

Indexed as

Animalsbeta CateninCadherinsCell ProliferationCyclin DFemaleGlucoseGreen Fluorescent ProteinsInsulin-Secreting CellsMaleMiceMice, TransgenicOligonucleotides, Antisensebeta CateninCadherinsCyclin DGlucoseGreen Fluorescent ProteinsOligonucleotides, Antisense

Identifiers

PMID23354125
PMCPMC3927460
OpenAlexW1974090169

What OpenQuestion holds

Textmetadata
LicenceTDM
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.