2018 Fiscal Year Final Research Report
Regulation mechanism of obesity by eicosanoids and development of therapeutic strategy
| Project/Area Number |
16K08256
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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 |
Biological pharmacy
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| Research Institution | Osaka University of Pharmaceutical Sciences |
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Principal Investigator |
Fujimori Ko 大阪薬科大学, 薬学部, 教授 (70425453)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | 肥満 / エイコサノイド |
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| Outline of Final Research Achievements |
We investigated the function of lipid mediators in the regulation of obesity. We constructed adipose-specific prostaglandin (PG) D2 synthase gene knockout (PGDS-KO) mice and analyzed the effect in obesity. Body weight gain was suppressed about 20% and insulin sensitivity was improved in adipocyte-specific PGDS-KO mice under high fat-diet. Moreover, the expression of the inflammatory-related genes was repressed in these mice. Thus, these results indicate that inhibition of PGD2 synthesis in adipocytes contributes to suppress obesity and to improve insulin sensitivity.
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| Free Research Field |
脂質生化学
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| Academic Significance and Societal Importance of the Research Achievements |
肥満は多くの生活習慣病の発症原因とされ、肥満の解消や防止は重要な課題である。本研究において、肥満制御における脂質の機能を解析したところ、脂肪細胞においてPGD2の合成を抑制することにより肥満は抑制され、インスリン感受性も改善された。よって、脂肪細胞においてPGD2の産生を抑制あるいは、PGD2の受容体の機能を阻害することにより肥満が抑制されることから、これらの調節薬は抗肥満薬となることが期待される。
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