| Project/Area Number |
26253058
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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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 |
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| Co-Investigator(Renkei-kenkyūsha) |
IWABU Masato 東京大学, 医学部附属病院, 特任准教授 (30557236)
IWABU Miki 東京大学, 医学部附属病院, 特任講師 (70392529)
KADOWAKI Takashi 東京大学, 医学部附属病院, 教授 (30185889)
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| Project Period (FY) |
2014-06-27 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥42,770,000 (Direct Cost: ¥32,900,000、Indirect Cost: ¥9,870,000)
Fiscal Year 2016: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2015: ¥7,930,000 (Direct Cost: ¥6,100,000、Indirect Cost: ¥1,830,000)
Fiscal Year 2014: ¥28,470,000 (Direct Cost: ¥21,900,000、Indirect Cost: ¥6,570,000)
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| Keywords | 糖尿病 / 細菌 / シグナル伝達 / 脂質 / 食品 |
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| Outline of Final Research Achievements |
We tried to clarify the mechanisms by which high-fat diet results in life-style related diseases, especially we studied interactions between immune cells and metabolism cells as well as gut microbiota and enteral metabolites. We analyzed the effects of high-fat diet, reduction in adiponectin/AdipoR actions, AdipoR activation, and transplantation of gut microbiota from AdipoR deficient mice into germfree mice. Our results raised the possibility that reduction in AdipoR actions could result in increased inflammation and oxidative stress and so on, leading to dysregulation of gut microbiota and enteral metabolites, which could worsen fatty liver, NASH, atherosclerosis, conversely AdipoR activation could ameliorate them.
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