| Project/Area Number |
14370334
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
ASANO Tomoichiro The University of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (70242063)
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| Co-Investigator(Kenkyū-buntansha) |
FIJISHIRO Midori The University of Tokyo, Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
OGIHARA Takehide The University of Tokyo, Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
TSUKADA Katsunori The University of Tokyo, Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
SHOUJIMA Nobuhiro The University of Tokyo, Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
ABE Miho The University of Tokyo, Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥15,000,000 (Direct Cost: ¥15,000,000)
Fiscal Year 2003: ¥5,800,000 (Direct Cost: ¥5,800,000)
Fiscal Year 2002: ¥9,200,000 (Direct Cost: ¥9,200,000)
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| Keywords | Insulin resistance / Diabetes / signal transduction / resistin / 糖代謝 / インスリン / Akt / AMPK |
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| Research Abstract |
It is well known that excessive salt intake induces elevation of blood pressure and that hypertension often coexists with insulin resistance. The contribution made by salt intake to the development of insulin resistance remains unclear, however. In this minireview, the insulin resistance seen in three salt-sensitive rat models (the high-salt-fed Sprague-Dawley rat, the Dahl salt sensitive rat and the chronically angiotensin II (AII)-infused rat) are presented. One notable observation common to all three models was that, despite their insulin-resistance, the early insulin signaling steps leading from activation of IR and IRSs to activation of PI 3-kinase Akt were apparently enhanced. This suggests that the molecular mechanism underlying the insulin resistance related to the salt-sensitive hypertension is unique. Other factors known to cause insulin resistance -e.g., obesity -actually suppress early insulin signaling, but for insulin resistance related to high salt intake, the impaired step must be further downstream in the insulin signaling pathway. What's more, increased oxidative stress appears to be crucially involved in both MI-and high-salt-induced insulin resistance.
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