| Project/Area Number |
15K08230
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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 |
General pharmacology
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
南 学 京都大学, 医学研究科, 准教授 (90511907)
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| Co-Investigator(Renkei-kenkyūsha) |
KAMEI Kaeko 京都工芸繊維大学, 工芸科学研究科, 教授 (00214544)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | プロスタグランジン / マクロファージ / 慢性炎症 / 糖代謝 |
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| Outline of Final Research Achievements |
With increasing body weight, macrophages accumulate in adipose tissue, giving rise to chronic inflammation and insulin resistance. In this study, we treated db/db mice with a prostaglandin E2 type 4 receptor (EP4) -selective agonist to explore the role of EP4 signaling in obesity-related inflammation. In the EP4 agonist-treated group, glucose tolerance and insulin resistance were significantly improved. Administration of the EP4 agonist inhibited the accumulation of F4/80-positive macrophages and the formation of crown-like structures, but increased the number of anti-inflammatory M2 macrophages in adipose tissue. In vitro M1/M2 polarization assay showed that treatment with EP4 agonist enhanced M2 polarization in wild-type peritoneal macrophages, whereas EP4-deficient macrophages were less susceptible to M2 polarization. Thus, EP4 signaling plays a critical role in obesity-related adipose tissue inflammation by regulating macrophage recruitment and polarization.
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