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Investigation of the mechanism by which TCF7L2 gene develops Type 2 diabetes

Research Project

Project/Area Number 20790639
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeSingle-year Grants
Research Field Metabolomics
Research InstitutionThe University of Tokyo

Principal Investigator

HORIKOSHI Momoko  The University of Tokyo, 医学部附属病院, 助教 (70422300)

Research Collaborator TAKAMOTO Iseki  東京大学, 医学部付属病院
Project Period (FY) 2008 – 2009
Project Status Completed (Fiscal Year 2009)
Budget Amount *help
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords2型糖尿病 / 遺伝子 / インスリン分泌
Research Abstract

TCF7L2 gene is widely accepted as a type 2 diabetes (T2D)-associated gene, the mechanism through which, however, is not well known. Thus we investigated its correlation with glucose metabolism by generating a TCF7L2 knock-down mouse with decreased function of TCF7L2 in the pancreatic beta cell. Glucose level of the TCF7L2 knock-down mouse during oral glucose tolerance test (OGTT) was significantly higher compared to the wild type mouse, and its insulin level was lower. Likewise, in human subjects who were homozygous for the T2D risk allele of TCF7L2rs7903146, the glucose levels at 90 min were significantly higher and the insulin levels at 120 min were significantly lower compared to the subjects with no risk allele during 75gOGTT. In conclusion, we demonstrated that the decrease of TCF7L2 function in the pancreatic beta cell will cause glucose intolerance through decreased insulin secretion.

Report

(3 results)
  • 2009 Annual Research Report   Final Research Report ( PDF )
  • 2008 Annual Research Report
  • Research Products

    (8 results)

All 2010 2009

All Presentation (8 results)

  • [Presentation] 膵β細胞のTcf7l2は膵β細胞量維持に重要な役割を果たしている2010

    • Author(s)
      高本偉碩
    • Organizer
      第83回日本内分泌学会学術総会
    • Place of Presentation
      京都
    • Year and Date
      2010-03-26
    • Related Report
      2009 Final Research Report
  • [Presentation] 膵β細胞のTcf712は膵β細胞量維持に重要な役割を果たしている2010

    • Author(s)
      高本偉碩
    • Organizer
      第83回日本内分泌学会学術総会
    • Place of Presentation
      京都
    • Year and Date
      2010-03-26
    • Related Report
      2009 Annual Research Report
  • [Presentation] 膵β細胞のTcf7l2は膵β細胞量維持に重要な役割を果たしている2010

    • Author(s)
      高本偉碩
    • Organizer
      第24回日本糖尿病・肥満動物学会年次学術集会
    • Place of Presentation
      大阪
    • Year and Date
      2010-01-22
    • Related Report
      2009 Final Research Report
  • [Presentation] 膵β細胞のTcf712は膵β細胞量維持に重要な役割を果たしている2010

    • Author(s)
      高本偉碩
    • Organizer
      第24回日本糖尿病・肥満動物学会年次学術集会
    • Place of Presentation
      大阪
    • Year and Date
      2010-01-22
    • Related Report
      2009 Annual Research Report
  • [Presentation] β細胞にdominant negative型Tcf7l2を過剰発現させたマウスは耐糖能異常を呈する2009

    • Author(s)
      高本偉碩膵
    • Organizer
      第59回日本体質医学会総会
    • Place of Presentation
      東京
    • Year and Date
      2009-07-26
    • Related Report
      2009 Final Research Report
  • [Presentation] 膵β細胞に dominant negative 型Tcf712を過剰発現させたマウスは耐糖能異常を呈する2009

    • Author(s)
      高本偉碩
    • Organizer
      第59回日本体質医学会総会
    • Place of Presentation
      東京
    • Year and Date
      2009-07-26
    • Related Report
      2009 Annual Research Report
  • [Presentation] 膵β細胞にdominant negative型Tcf7l2を過剰発現させたマウスは耐糖能異常を呈する2009

    • Author(s)
      高本偉碩
    • Organizer
      第52回日本糖尿病学会年次学術集会
    • Place of Presentation
      大阪
    • Year and Date
      2009-05-23
    • Related Report
      2009 Final Research Report
  • [Presentation] 膵β細胞に dominant negative 型Tcf712を過剰発現させたマウスは耐糖能異常を呈する2009

    • Author(s)
      高本偉碩
    • Organizer
      第52回日本糖尿病学会年次学術集会
    • Place of Presentation
      大阪
    • Year and Date
      2009-05-23
    • Related Report
      2009 Annual Research Report

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Published: 2008-04-01   Modified: 2016-04-21  

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