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Study · Animal study (in vivo) · mouse · 2010

10 results

Inhibition of monocyte adhesion to endothelial cells and attenuation of atherosclerotic lesion by a glucagon-like peptide-1 receptor agonist, exendin-4.

Arakawa M, Mita T, Azuma K, Ebato C, Goto H, Nomiyama T, Fujitani Y, Hirose T, Kawamori R, Watada H

Diabetes12 Jan 2010Cited by 467 (Europe PMC)

PMID20068138 (opens in a new tab)PMCIDPMC2844811 (opens in a new tab)DOI10.2337/db09-1694 (opens in a new tab)PepBankPUB-20068138
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study10

8 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Mechanism

    In C57BL/6 mice, exendin‑4 inhibited monocyte adhesion in the aorta.

    In plain wordsIn mice, exendin‑4 reduced monocyte adhesion in the aorta.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseAortic monocyte adhesion
    Study

    mousen: not reported in source

    C57BL/6 mice
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    300 pmol/kg/day or 24 nmol/kg/day · continuous infusionAs given in this study (mouse).

    Source sentences

    Summary
    Treatment with exendin-4 significantly inhibited monocytic adhesion in the aortas of C57BL/6 mice without affecting metabolic parameters.
    1 context sentence
    Summary · context
    After continuous infusion of low (300 pmol . kg(-1) . day(-1)) or high (24 nmol . kg(-1) . day(-1)) dose of exendin-4 in C57BL/6 or apolipoprotein E-deficient mice (apoE(-/-)), we evaluated monocyte adhesion to the endothelia of thoracic aorta and arteriosclerotic lesions around the aortic valve.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In C57BL/6 mice, exendin‑4 did not affect metabolic parameters.

    In plain wordsIn mice, exendin‑4 did not change metabolic measurements.

    Peptide
    Exenatide (exendin-4)
    Outcome
    No significant changeMetabolic parameters
    Study

    mousen: not reported in source

    C57BL/6 mice
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    300 pmol/kg/day or 24 nmol/kg/day · continuous infusionAs given in this study (mouse).

    Source sentences

    Summary
    Treatment with exendin-4 significantly inhibited monocytic adhesion in the aortas of C57BL/6 mice without affecting metabolic parameters.
    1 context sentence
    Summary · context
    After continuous infusion of low (300 pmol . kg(-1) . day(-1)) or high (24 nmol . kg(-1) . day(-1)) dose of exendin-4 in C57BL/6 or apolipoprotein E-deficient mice (apoE(-/-)), we evaluated monocyte adhesion to the endothelia of thoracic aorta and arteriosclerotic lesions around the aortic valve.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In apolipoprotein E-deficient mice, exendin‑4 reduced monocyte adhesion to the endothelium.

    In plain wordsIn mice lacking apolipoprotein E, exendin‑4 reduced monocyte adhesion to blood vessel linings.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseEndothelial monocyte adhesion
    Study

    mousen: not reported in source

    Apolipoprotein E-deficient mice
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    300 pmol/kg/day or 24 nmol/kg/day · continuous infusionAs given in this study (mouse).

    Source sentences

    Summary
    In apoE(-/-) mice, the same treatment reduced monocyte adhesion to the endothelium and suppressed atherosclerogenesis.
    1 context sentence
    Summary · context
    After continuous infusion of low (300 pmol . kg(-1) . day(-1)) or high (24 nmol . kg(-1) . day(-1)) dose of exendin-4 in C57BL/6 or apolipoprotein E-deficient mice (apoE(-/-)), we evaluated monocyte adhesion to the endothelia of thoracic aorta and arteriosclerotic lesions around the aortic valve.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In apolipoprotein E-deficient mice, exendin‑4 suppressed atherosclerogenesis.

    In plain wordsIn mice lacking apolipoprotein E, exendin‑4 reduced atherosclerosis development.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseAtherosclerogenesis
    Study

    mousen: not reported in source

    Apolipoprotein E-deficient mice
    Outcome group
    Cardiovascular events · Cardiovascular
    Studied dose
    300 pmol/kg/day or 24 nmol/kg/day · continuous infusionAs given in this study (mouse).

    Source sentences

    Summary
    In apoE(-/-) mice, the same treatment reduced monocyte adhesion to the endothelium and suppressed atherosclerogenesis.
    1 context sentence
    Summary · context
    After continuous infusion of low (300 pmol . kg(-1) . day(-1)) or high (24 nmol . kg(-1) . day(-1)) dose of exendin-4 in C57BL/6 or apolipoprotein E-deficient mice (apoE(-/-)), we evaluated monocyte adhesion to the endothelia of thoracic aorta and arteriosclerotic lesions around the aortic valve.
  5. 05LabIn vitro (cells)Mechanism

    In mouse macrophages, exendin‑4 suppressed lipopolysaccharide-induced TNF-alpha mRNA expression.

    In plain wordsIn cells from mice, exendin‑4 reduced lipopolysaccharide-induced TNF-alpha messenger RNA.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseTNF-alpha mRNA
    Study

    mousen: not reported in source

    Macrophages challenged with lipopolysaccharide
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro treatment of mouse macrophages with exendin-4 suppressed lipopolysaccharide-induced mRNA expression of tumor necrosis factor-alpha and monocyte chemoattractant protein-1, and suppressed nuclear translocation of p65, a component of nuclear factor-kappaB.
  6. 06LabIn vitro (cells)Mechanism

    In mouse macrophages, exendin‑4 suppressed lipopolysaccharide-induced monocyte chemoattractant protein-1 mRNA expression.

    In plain wordsIn cells from mice, exendin‑4 reduced lipopolysaccharide-induced monocyte chemoattractant protein-1 messenger RNA.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseMCP-1 mRNA
    Study

    mousen: not reported in source

    Macrophages challenged with lipopolysaccharide
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro treatment of mouse macrophages with exendin-4 suppressed lipopolysaccharide-induced mRNA expression of tumor necrosis factor-alpha and monocyte chemoattractant protein-1, and suppressed nuclear translocation of p65, a component of nuclear factor-kappaB.
  7. 07LabIn vitro (cells)Mechanism

    In mouse macrophages, exendin‑4 suppressed nuclear translocation of p65.

    In plain wordsIn cells from mice, exendin‑4 reduced movement of p65 into cell nuclei.

    Peptide
    Exenatide (exendin-4)
    Outcome
    Decreasep65 nuclear translocation
    Study

    mousen: not reported in source

    Macrophages challenged with lipopolysaccharide
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro treatment of mouse macrophages with exendin-4 suppressed lipopolysaccharide-induced mRNA expression of tumor necrosis factor-alpha and monocyte chemoattractant protein-1, and suppressed nuclear translocation of p65, a component of nuclear factor-kappaB.
  8. 08LabIn vitro (cells)Mechanism

    In human monocytes, exendin‑4 reduced CD11b expression.

    In plain wordsIn cells, exendin‑4 reduced CD11b expression in human monocytes.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseCD11b expression
    Study

    humann: not reported in source

    Human monocytes
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In human monocytes, exendin-4 reduced the expression of CD11b.

Studies that did not test the peptide alone2

In this study, Exenatide (exendin-4) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Exenatide (exendin-4).

  1. 09LabNot a test of Exenatide (exendin-4) aloneIn vitro (cells)Mechanism

    In mouse macrophages, the cAMP inhibitor MDL-12330A reversed the reported suppressive effect of exendin‑4.

    In plain wordsIn cells from mice, a cAMP inhibitor reversed the reported suppressive effect of exendin‑4.

    Peptide
    Exenatide (exendin-4)
    Outcome
    MixedReversal by cAMP inhibition
    Study

    mousen: not reported in source

    Mouse macrophages
    Outcome group
    Inflammation markers · Cardiovascular

    Source sentences

    Summary
    This effect was reversed by either MDL-12330A, a cAMP inhibitor or PKI(14-22), a protein kinase A-specific inhibitor.
    1 context sentence
    Summary · context
    In vitro treatment of mouse macrophages with exendin-4 suppressed lipopolysaccharide-induced mRNA expression of tumor necrosis factor-alpha and monocyte chemoattractant protein-1, and suppressed nuclear translocation of p65, a component of nuclear factor-kappaB.

    In this study, Exenatide (exendin-4) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Exenatide (exendin-4).

  2. 10LabNot a test of Exenatide (exendin-4) aloneIn vitro (cells)Mechanism

    In mouse macrophages, the protein kinase A inhibitor PKI(14-22) reversed the reported suppressive effect of exendin‑4.

    In plain wordsIn cells from mice, a protein kinase A inhibitor reversed the reported suppressive effect of exendin‑4.

    Peptide
    Exenatide (exendin-4)
    Outcome
    MixedReversal by protein kinase A inhibition
    Study

    mousen: not reported in source

    Mouse macrophages
    Outcome group
    Inflammation markers · Cardiovascular

    Source sentences

    Summary
    This effect was reversed by either MDL-12330A, a cAMP inhibitor or PKI(14-22), a protein kinase A-specific inhibitor.
    1 context sentence
    Summary · context
    In vitro treatment of mouse macrophages with exendin-4 suppressed lipopolysaccharide-induced mRNA expression of tumor necrosis factor-alpha and monocyte chemoattractant protein-1, and suppressed nuclear translocation of p65, a component of nuclear factor-kappaB.

    In this study, Exenatide (exendin-4) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Exenatide (exendin-4).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Registered trials1

Trials this study reports on, or that list this study as a reference. Registry data from ClinicalTrials.gov.

1 trial · source ClinicalTrials.gov (opens in a new tab)

Status unknownPhase 4NCT04122716

Combined Effects of GLP-1 Analogue and Exercise on Maintenance of Weight Loss and Health After Very-low Calorie Diet

Signe Torekovn = 215Sept 2016 to est. Nov 2021

Obesity

Trial pageClinicalTrials.govUpdated 2 Nov 2020

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    22 Oct 2026, 02:26 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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