| Project/Area Number |
16K19546
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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 | Keio University |
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Principal Investigator |
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| Research Collaborator |
Itoh Hiroshi 慶應義塾大学, 医学部, 教授 (40252457)
Nakae Jun 慶應義塾大学, 医学部, 准教授 (00344573)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | インスリン抵抗性 / 腸管免疫 / 肥満 / 糖尿病 / マクロファージ / 樹状細胞 / T細胞 |
|---|
| Outline of Final Research Achievements |
Foxo1 is important in regulating glucose and energy homeostasis, but little is known about the roles in intestinal T cell under HFD. We generated CD4 T cell specific Foxo1 double Foxo3 hetero-KO(T-QKO) mice, Insulin sensitivity of T-QKO mice was significantly improved compared with control mice. Gene expression of Il4 and Il13 in Peyer’s patch from T-QKO were significantly increased compared with control mice. These data suggested that Foxo activation of CD4+Tcell may deteriorate HFD induced insulin resistance. Nlrp10 is known as NLR family and it has been reported that Nlrp10 in Dendritic Cell play important roles in T cell activation and induction of Acquired Immunity.Insulin sensitivity of CD11cNlrp10KO was significantly deteriorated compared with control mice. Gene expression of Foxo3 and Il17 in colon from Nlrp10KO were decreased compared with HFD control mice. These data suggested that Nlrp10 in Dendritic cell may play protective roles in HFD induced insulin resistance
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