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Related Concept Videos

  • Biomedical And Clinical Sciences
  • Oncology And Carcinogenesis
  • Predictive And Prognostic Markers
  • Adiponectin Deficiency Protects Mice From Chemically Induced Colonic Inflammation.
  • Biomedical And Clinical Sciences
  • Oncology And Carcinogenesis
  • Predictive And Prognostic Markers
  • Adiponectin Deficiency Protects Mice From Chemically Induced Colonic Inflammation.

    • Related Experiment Videos

    Adiponectin deficiency protects mice from chemically induced colonic inflammation.

    Raja Fayad1, Maria Pini, Joseph A Sennello

    • 1Department of Human Nutrition, University of Illinois at Chicago, 60612, USA.

    Gastroenterology
    |January 30, 2007

    View abstract on PubMed

    Summary
    This summary is machine-generated.

    Adiponectin (APN) deficiency protects against intestinal inflammation. APN promotes inflammation by increasing cytokines and inhibiting protective growth factors in the colon, unlike its anti-inflammatory role in atherosclerosis.

    Related Experiment Videos

    Area of Science:

    • Gastroenterology
    • Immunology
    • Endocrinology

    Background:

    • Adiponectin (APN) is an adipokine known for its insulin-sensitizing and anti-inflammatory properties, particularly in atherosclerosis.
    • Its specific role in intestinal inflammation, however, remained largely unexplored.

    Purpose of the Study:

    • To investigate the function of adiponectin (APN) in the context of intestinal inflammation.
    • To elucidate the mechanisms by which APN influences colitis.

    Main Methods:

    • Utilized adiponectin knockout (KO) mice and wild-type (WT) littermates subjected to chemically induced colitis (DSS and TNBS models).
    • Assessed clinical and histologic scores, epithelial cell proliferation, cytokine levels, and APN expression.
    • Analyzed the expression and interaction of APN with growth factors like HB-EGF and bFGF using immunohistochemistry, RT-PCR, and coimmunoprecipitation.

    Main Results:

    • Adiponectin knockout mice exhibited protection against chemically induced colitis, with APN administration restoring inflammation.
    • APN was found to be expressed in the colon and associated with epithelial cells.
    • In vitro studies demonstrated that APN enhances proinflammatory cytokine production and inhibits the protective activity of HB-EGF and bFGF by binding to them.

    Conclusions:

    • Adiponectin deficiency confers protection from chemically induced colitis.
    • APN promotes intestinal inflammation by increasing proinflammatory cytokines and suppressing protective growth factors, such as HB-EGF and bFGF.
    • The role of APN in colitis is proinflammatory, contrasting with its anti-inflammatory effects in atherosclerosis.