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Elucidation of the mechanism of metabolic syndrome due to the gene targeting analysis of the causative gene

Research Project

Project/Area Number 23591300
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Metabolomics
Research InstitutionThe University of Tokyo

Principal Investigator

IIZUKA Yoko  東京大学, 医学部附属病院, 助教 (40420244)

Co-Investigator(Kenkyū-buntansha) YAHAGI Naoya  筑波大学, 医学医療系, 准教授 (60420246)
Project Period (FY) 2011 – 2013
Project Status Completed (Fiscal Year 2013)
Budget Amount *help
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Keywordsメタボリックシンドローム / インスリン抵抗性 / 高血圧 / 交感神経活動亢進 / 原因候補遺伝子 / 高血圧自然発症ラットSHR / ノックアウトマウス / 尿崩症 / 肥満
Research Abstract

[Purpose and methods] Through the gene targeting analysis of KAT-1, I explore the origin of metabolic syndrome and its physiological function. [Results and conclusions] As with the SHR, KAT-1 knockout mice exhibited an increase in blood pressure and heart rate significant in a normal diet and 12 weeks high salt diet, exhibited enhanced catecholamine secretion of 24-hour urine in high salt diet, showed an increase in plasma aldosterone concentration and a decreased in renin activity, showed a significant increase in fasting blood glucose levels and the enhancement of insulin resistance by insulin tolerance test in normal diet. Along with the increase in activity, and showed a decrease in the rate of increase in body weight, adipose tissue weight in the high-fat diet. It was strongly suggested that KAT-1 is a potential new therapeutic targets for metabolic syndrome.

Report

(4 results)
  • 2013 Annual Research Report   Final Research Report ( PDF )
  • 2012 Research-status Report
  • 2011 Research-status Report
  • Research Products

    (3 results)

All 2011

All Presentation (3 results)

  • [Presentation] SHRのメタボリックシンドローム原因候補遺伝子(KAT-1)の欠損マウスを用いた生理的機能の解明2011

    • Author(s)
      飯塚陽子,大須賀淳一,喬荊,武内謙憲,高瀬暁,高梨幹生,西真貴子,久保田みどり,升田紫,熊谷真義,太田啓介,山本隆史,泉田欣彦,矢作直也,大橋健,島野仁,石橋俊,藤田敏郎,山田信博,後藤田貴也,門脇孝
    • Organizer
      第54回日本糖尿病学会年次学術集会
    • Place of Presentation
      札幌
    • Related Report
      2013 Final Research Report 2011 Research-status Report
  • [Presentation] SHRのメタボリックシンドローム原因候補遺伝子(KAT-1)欠損マウスを用いたその生理的機能の解明2011

    • Author(s)
      飯塚陽子,喬荊,大須賀淳一,武内謙憲,高瀬暁,高梨幹生,西真貴子,久保田みどり,升田紫,熊谷真義,太田啓介,山本隆史,泉田欣彦,矢作直也,大橋健,島野仁,石橋俊,藤田敏郎,山田信博,後藤田貴也,門脇孝
    • Organizer
      第26回日本糖尿病合併症学会
    • Place of Presentation
      大宮
    • Related Report
      2013 Final Research Report
  • [Presentation] SHRのメタボリックシンドローム原因候補遺伝子(KAT-1)欠損マウスを用いたその生理的機能の解明2011

    • Author(s)
      飯塚 陽子、他
    • Organizer
      第26回日本糖尿病合併症学会
    • Place of Presentation
      大宮
    • Related Report
      2011 Research-status Report

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Published: 2011-08-05   Modified: 2019-07-29  

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