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The role of mesenteric lymph node on visceral fat accumulation and metabolic disorders

Research Project

Project/Area Number 25670434
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Metabolomics
Research InstitutionOsaka University

Principal Investigator

SHIMOMURA IICHIRO  大阪大学, 医学(系)研究科(研究院), 教授 (60346145)

Co-Investigator(Kenkyū-buntansha) FUKUHARA Atsunori  大阪大学, 医学系研究科, 助教 (00437328)
Project Period (FY) 2013-04-01 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords腸間膜脂肪 / アディポネクチン / 腸間膜リンパ節 / Treg / アディポネクチン / メタボリックシンドローム / 内臓脂肪 / 糖尿病 / 肥満
Outline of Final Research Achievements

Accumulation of visceral WATs causes abnormalities in glucose and lipid metabolism resulting in atherosclerosis and cardiovascular diseases. Mesenteric lymph node (MLN) is located in the base of mesenteric WAT. The aim of this study is to reveal the significance of mesenteric lymph node against inflammation and metabolic disorders.
Mesenteric lymph nodes are removed in male C57BL/6J mice {MLNrem mice}, and glucose tolerance and markers of immune cells were compared to sham-operated mice (sham mice). MLNrem mice showed impaired glucose tolerance compared to sham mice. Number of macrophages was increased in mesenteric WAT of MLNrem mice, and further induced by feeding of high-fat diet. Expression of marker genes of Treg was decreased in MLNrem mice. Collectively, MLN is important to protect mesenteric WATs from inflammation by inducing Tregs and inhibiting infiltration of macrophage, and maintain glucose homeostasis.

Report

(4 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2014 Research-status Report
  • 2013 Research-status Report
  • Research Products

    (5 results)

All 2016 2015 2014

All Journal Article (1 results) (of which Peer Reviewed: 1 results,  Open Access: 1 results,  Acknowledgement Compliant: 1 results) Presentation (4 results) (of which Int'l Joint Research: 1 results)

  • [Journal Article] Adipose tissue macrophages induce PPARγ-high FOXP3(+) regulatory T cells.2015

    • Author(s)
      Onodera T, Fukuhara A, Jang MH, Shin JH, Aoi K, Kikuta J, Otsuki M, Ishii M, Shimomura I.
    • Journal Title

      Scientific Reports

      Volume: 5 Pages: 1-12

    • Related Report
      2015 Annual Research Report
    • Peer Reviewed / Open Access / Acknowledgement Compliant
  • [Presentation] Adipose tissue macrophages induce PPARγ-high FOXP3+ regulatory T cells2016

    • Author(s)
      小野寺俊晴、福原淳範、大月道夫、下村伊一郎
    • Organizer
      Keystone SYMPOSIA Obesity and Adipose Tissue Biology
    • Place of Presentation
      カナダ バンフ
    • Year and Date
      2016-02-17
    • Related Report
      2015 Annual Research Report
    • Int'l Joint Research
  • [Presentation] 脂肪組織マクロファージはPPARγ陽性調節性T細胞(Treg)を誘導する2015

    • Author(s)
      小野寺俊晴、福原淳範、張 明浩、北村哲宏、大月道夫、下村伊一郎
    • Organizer
      第58回日本糖尿病学会年次学術集会
    • Place of Presentation
      山口県
    • Year and Date
      2015-05-21
    • Related Report
      2015 Annual Research Report
  • [Presentation] 脂肪細胞マクロファージはアディポネクチンによって維持され、PPARγ陽性調節性T細胞を誘導する2014

    • Author(s)
      小野寺俊晴、福原淳範、北村哲宏、大月道夫、下村伊一郎
    • Organizer
      第19回 アディポサイエンス・シンポジウム
    • Place of Presentation
      大阪
    • Year and Date
      2014-08-23
    • Related Report
      2014 Research-status Report
  • [Presentation] 脂肪組織マクロファージによる調節性T細胞誘導2014

    • Author(s)
      小野寺俊晴
    • Organizer
      第57回 日本糖尿病学会年次学術集会
    • Place of Presentation
      大阪
    • Year and Date
      2014-05-24
    • Related Report
      2014 Research-status Report

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Published: 2014-07-25   Modified: 2019-07-29  

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