| Project/Area Number |
26861816
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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 |
Periodontology
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | CCL19 / CCR7 / 脂肪組織 / インスリン抵抗性 / 樹状細胞 / ccl19 / 脂肪細胞 / マクロファージ |
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| Outline of Final Research Achievements |
This study aimed to evaluate the role of CCL19-CCR7 axis on obesity and insulin resistance. CCL19 protein was elevated in the sera of obese model mice challenged by endotoxin. Ccr7(-/-) mice were protected from diet-induced obesity, insulin resistance, fatty liver and dyslipidemia and exhibited increased thermogenesis on high-fat feeding. CCL19 attracts activated dendritic cells. The expression of dendritic cell markers, CD11b and CD11c, was not observed in the adipose tissues of Ccr7(-/-) mice fed a high-fat diet, which might be closely associated with the protection of these mice from obesity.
In this study, we demonstrated that CCL19-CCR7 pathway played a crucial role in inducing obesity and subsequent insulin resistance.
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