| Project/Area Number |
23591300
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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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 |
IIZUKA Yoko 東京大学, 医学部附属病院, 助教 (40420244)
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| Co-Investigator(Kenkyū-buntansha) |
YAHAGI Naoya 筑波大学, 医学医療系, 准教授 (60420246)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| 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)
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| 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 |
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| 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.
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