Evidence map›Paper›PMID 21307078›Full record

ArticleDiabetes2011

Glucose and inflammation control islet vascular density and beta-cell function in NOD mice: control of islet vasculature and vascular endothelial growth factor by glucose.

Eitan M Akirav, Maria-Teresa Baquero, Lynn W Opare-Addo, Michael Akirav, Eva Galvan, Jake A Kushner, David L Rimm, Kevan C Herold

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
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  4. Review
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  6. Article
  7. Type 1 diabetes.Lancet (London, England) · 2018
    Review
  8. Article
  9. Article
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  11. Review
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  13. Review
  14. Article
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  16. 3-Dimensional histological reconstruction and imaging of the murine pancreas.Mammalian genome : official journal of the International Mammalian Genome Society · 2014
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

8 authors at 3 institutions in 2 countries.

Eitan M AkiravDepartment of Immunobiology and Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA. eitan.akirav@yale.edu
Maria-Teresa Baquero
Lynn W Opare-Addo
Michael Akirav
Eva Galvan
Jake A Kushner
David L Rimm
Kevan C Herold
Yale University · USBar-Ilan University · ILChildren's Hospital of Philadelphia · US

Funding

Phase II Trial of HOKT3gamma 1 (ALA-ALA) in Type 1 DiabetesR01DK057846 · NIDDK · YALE UNIVERSITY · PI Kevan C Herold · 2000 to 2026
$11.1M
NIDDK NIH HHS DK-057846NIDDK NIH HHS R01 DK057846
6 · The paper itself

Abstract

objectiveβ-Cell and islet endothelial cell destruction occurs during the progression of type 1 diabetes, but, paradoxically, β-cell proliferation is increased during this period. Altered glucose tolerance may affect β-cell mass and its association with endothelial cells. Our objective was to study the effects of glucose and inflammation on islet vascularity and on β function, mass, and insulin in immunologically tolerant anti-CD3 monoclonal antibody (mAb)-treated and prediabetic NOD mice. RESEARCH DESIGN AND

methodsThe effects of phloridzin or glucose injections on β-cells and endothelial cells were tested in prediabetic and previously diabetic NOD mice treated with anti-CD3 mAbs. Glucose tolerance, immunofluorescence staining, and examination of islet cultures ex vivo were evaluated.

resultsIslet endothelial cell density decreased in NOD mice and failed to recover after anti-CD3 mAb treatment despite baseline euglycemia. Glucose treatment of anti-CD3 mAb-treated mice showed increased islet vascular density and increased insulin content, which was associated with improved glucose tolerance. The increase in the vascular area was dependent on islet inflammation. Increased islet endothelial cell density was associated with increased production of vascular endothelial growth factor (VEGF) by islets from NOD mice. This response was recapitulated ex vivo by the transfer of supernatants from NOD islets cultured in high-glucose levels.

conclusionsOur results demonstrate a novel role for glucose and inflammation in the control of islet vasculature and insulin content of β-cells in prediabetic and anti-CD3-treated NOD mice. VEGF production by the islets is affected by glucose levels and is imparted by soluble factors released by inflamed islets.

Indexed as

AnimalsDiabetes Mellitus, Type 1Fluorescent Antibody TechniqueGlucoseInflammationInsulin-Secreting CellsIslets of LangerhansMiceMice, Inbred NODReverse Transcriptase Polymerase Chain ReactionVascular Endothelial Growth Factor AGlucoseVascular Endothelial Growth Factor A

Identifiers

PMID21307078
PMCPMC3046848
OpenAlexW2144858797

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.