| Project/Area Number |
26350166
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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 |
Eating habits
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| Research Institution | Kobe Gakuin University |
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Principal Investigator |
Hideo Ohira 神戸学院大学, 栄養学部, 准教授 (40351762)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2016: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | Butyrate / Adipocyte / Macrophage / Lipolysis / Prostaglandin E2 / Short chain fatty acid / 酪酸 / 脂肪細胞 / マクロファージ / 短鎖脂肪酸 / プロスタグランディンE2 |
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| Outline of Final Research Achievements |
Using contact or transwell co-culture methods with differentiated 3T3-L1 and RAW264.7, we examined sodium butyrate (Bt), PGE2 and involved lipolysis mechanisms. Bt significantly increased PGE2 production compared with co-culture. In this mechanisms, Bt elevated COX2 expression in macrophages and adipocytes, cPLA2 activity in macrophages compared with co-culture. As for lipolysis, co-culture increased lipolysis, whereas butyrate and PGE2 suppressed it. The PGE receptor 3 antagonist reversed the control level in PGE2 treated cells and partially reversed the control in butyrate treated cells. It is suggested butyrate may attenuate lipolysis in adipocytes co-cultured with macrophages via PGE2 mediated and non-PGE2 mediated pathways.
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