Evidence map›Paper›PMID 20635178›Full record

ArticleDiabetologia2010

Anti-inflammatory action of exendin-4 in human islets is enhanced by phosphodiesterase inhibitors: potential therapeutic benefits in diabetic patients.

U Pugazhenthi, K Velmurugan, A Tran, G Mahaffey, S Pugazhenthi

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In one paragraph

Article in Diabetologia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. The Regulation Role of the Gut-Islets Axis in Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  6. Review
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  8. Review
  9. Article
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  12. Autocrine Interleukin-10 Mediates Glucagon-Like Peptide-1 Receptor-Induced Spinal Microglial β-Endorphin Expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  13. Article
  14. Article
  15. GLP-1 nanomedicine alleviates gut inflammation.Nanomedicine : nanotechnology, biology, and medicine · 2017
    Article
  16. Article
  17. Review
  18. Review
  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

5 authors at 1 institution in 1 country.

U PugazhenthiDepartment of Medicine, University of Colorado Denver, Mail Stop 8106, 12801 E 17th Ave, Aurora, CO 80045, USA.
K Velmurugan
A Tran
G Mahaffey
S Pugazhenthi
Veterans Health Administration · US

Funding

BLRD VA I01 BX001837
6 · The paper itself

Abstract

aims/hypothesisExendin-4, a glucagon-like peptide-1 (GLP-1) analogue, is reported to have modest anti-inflammatory effects in addition to that of improving beta cell survival. We therefore sought to determine whether exendin-4 decreases expression of the gene encoding chemokine (C-X-C motif) ligand (CXCL)10, which plays a role in initiating insulitis in type 1 diabetes.

methodsThe expression of CXCL10 in human islets was determined at the mRNA level by real-time RT-PCR analysis and at the protein level by western blotting. The level of CXCL10 in culture medium was measured by ELISA. Pathway-specific gene expression profiling was carried out to determine the expression of a panel of genes encoding chemokines and cytokines in human islets exposed to cytokines.

resultsIFN-γ induced expression of CXCL10 through activation of signal transducer and activator of transcription-1 (STAT-1). A combination of cytokines (IL-1β, TNF-α and IFN-γ) showed strong synergy in the induction of numerous chemokines and cytokines through nuclear factor kappa B and STAT-1. Exendin-4 suppressed basal expression of several inflammatory mediators. In combination with phosphodiesterase inhibitors, exendin-4 also decreased IFN-γ-induced CXCL10 expression in human islets and in MIN6 cells (a mouse beta cell line), and its secretion into the culture medium. Exendin-4 action was mimicked by forskolin, an activator of adenylyl cyclase, and by dibutyryl cyclic AMP. Protein kinase A was not involved in mediating exendin-4 action on CXCL10. The mechanism of exendin-4's anti-inflammatory action involved decreases in STAT-1 levels. CONCLUSIONS/

interpretationThese findings suggest that the GLP-1-cyclic AMP pathway decreases islet inflammation in addition to its known effects on beta cell survival.

Indexed as

Analysis of VarianceAnti-Inflammatory AgentsBlotting, WesternCell LineCells, CulturedChemokine CXCL10Cyclic AMPDiabetes MellitusEnzyme-Linked Immunosorbent AssayExenatideHumansInterferon-gammaInterleukin-1betaIn Vitro TechniquesIslets of LangerhansNF-kappa BAnti-Inflammatory AgentsChemokine CXCL10CXCL10 protein, humanCyclic AMPExenatideInterferon-gammaInterleukin-1betaNF-kappa BPeptidesPhosphodiesterase InhibitorsRNA, MessengerSTAT1 protein, humanSTAT1 Transcription FactorTumor Necrosis Factor-alphaVenoms

Identifiers

PMID20635178
OpenAlexW2007907433

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.