| Project/Area Number |
26860162
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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 |
Environmental physiology(including physical medicine and nutritional physiology)
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| Research Institution | St. Marianna University School of Medicine |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ニューロペプチドY / GPER / エストロゲン / 視床下部 / GPR30 / G1 / G15 / Neuropeptide Y / 代謝 / 受容体 |
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| Outline of Final Research Achievements |
The present study was carried out to see possible involvement of G-protein-coupled estrogen receptor 1 (GPER, GPR30) in NPY neurons to glucose metabolism. Rats were ovariectomized and were primed with the silicone tube containing cholesterol or GPER selective agonist G1. Firstly, we revealed that G1 agonist did not have estrogenic action in reproductive system. Glucose tolerance test was worsened by G1 treatment in rats. In high fat fed mice, glucose tolerance was affected by G1 dose depending manner. These results suggested that GPER affect glucose metabolism in a manner different from via estrogen receptor-α and through NPY neurons. Since NPY neurons were identified by mVenus under fluorescent microscopy and this transgenic mice were expressed the human interleukin 2 receptor alpha subunit (IL-2R alpha) under the control of the NPY gene promoter. Thus treatment immunotoxin ablates conditionally NPY neurons.
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