| Project/Area Number |
25860745
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Metabolomics
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| Research Institution | Kanazawa University |
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Principal Investigator |
NAGASHIMADA Mayumi 金沢大学, 脳・肝インターフェースメディシン研究センター, 博士研究員 (30645510)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | ケモカイン / 慢性炎症 / インスリン抵抗性 / フラクタルカイン / CX3CR1 / 肥満 / fractalkine / マクロファージ / 脂肪組織 |
|---|
| Outline of Final Research Achievements |
The physiological and pathophysiological role of fractalkine and its receptor CX3CR1 in diseases are complex and not fully understood. In particular, it is not known how fractalkine-CX3CR1 can regulate obesity-associated chronic inflammation and metabolic diseases. Here, we investigated the role of fractalkine and CX3R1 system in obesity-induced inflammation and insulin resistance. We found that CX3CR1 deficient mice showed that insulin resistance, glucose intolerance, and hepatic steatosis in response to high fat (HF) feeding. These data suggested that fractalkine-CX3CR1 signal play a crucial role in development of insulin resistance. Further studies to clarify the mechanism by which fractalkine-CX3CR1 regulate inflammation and insulin resistance are going on.
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