第18回徳島医学会賞受賞論文 Cbl-b欠損によるマクロファージの活性化を介した耐糖能異常  [in Japanese] Deficiency of Cbl-b gene enhances infiltration and activation of macrophages in adipose tissue and causes peripheral insulin resistance in mice  [in Japanese]

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Abstract

Obesity is a major cause of insulin resistance and is considered a chronic low-grade inflammatory disease. Substantial evidence has accumulated in recent years that chronic infiltration and activation of macrophages in white adipose tissue underlie the obesity-related component of these insulin resistant states. In the present study, we examined the role of Cbl-b, ubiquitin ligase, in insulin action. Elderly Cbl-b-deficient mice(Cbl-b-/-mice)developed glucose intolerance and peripheral insulin resistance. Deficiency of Cbl-b gene was associated with infiltration of macrophages into the WAT and expression of cytokines, such as tumor necrosis factor-α, interleukin-6 and monocyte chemoattractant protein-1. Furthermore, Vav1, a key factor in macrophage activation, was highly phosphorylated in peritoneal Cbl-b-/-macrophages, compared with wild type macrophages, suggesting that Cbl-b deficiency induces macrophage activation. Our results suggest that Cbl-b is a negative regulator of macrophage activation, and that macrophage activation by Cbl-b deficiency, at least in part, contributes to the peripheral insulin resistance and glucose intolerance.

Journal

  • Shikoku acta medica

    Shikoku acta medica 63(3・4), 111-115, 2007-08-25

    徳島医学会

Codes

  • NII Article ID (NAID)
    120006324305
  • NII NACSIS-CAT ID (NCID)
    AN00102041
  • Text Lang
    JPN
  • Article Type
    journal article
  • Journal Type
    大学紀要
  • ISSN
    00373699
  • NDL Article ID
    8951956
  • NDL Source Classification
    ZS7(科学技術--医学)
  • NDL Call No.
    Z19-344
  • Data Source
    NDL  IR 
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