| Project/Area Number |
16H06616
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Eating habits
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| Research Institution | Tohoku University |
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Principal Investigator |
Yasumoto Yuki 東北大学, 医学系研究科, 助教 (40779352)
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| Co-Investigator(Renkei-kenkyūsha) |
OWADA YUJI 東北大学, 大学院医学系研究科, 教授 (20292211)
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| Project Period (FY) |
2016-08-26 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 視床下部 / グリア / オリゴデンドロサイト前駆細胞 / レプチン / エネルギー代謝 / 摂食行動 |
|---|
| Outline of Final Research Achievements |
In this study, we established OPC specific dysfunction mouse, performed morphological analysis by 3D electron microscopy and examined the role of fatty acid-binding protein 7 (FABP7) in the hypothalamic ARC. We performed a phenotypic analysis of diet-induced FABP7 knockout (KO) obese mice and of FABP7 KO mice treated with a single leptin injection. In mice fed a high-fat diet, weight gain and food intake were lower in FABP7 KO mice than in wild type (WT) mice. FABP7 KO mice also had lower food intake and weight gain after a single injection of leptin, and we consistently confirmed that the number of pSTAT3+ cells in the ARC indicated that the leptin-induced activation of neurons was significantly more frequent in FABP7 KO mice than in WT mice. These results indicate that in hypothalamic astrocytes, FABP7 might be involved in sensing neuronal leptin via glia-mediated mechanisms and plays a pivotal role in controlling systemic energy homeostasis.
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