| Project/Area Number |
15H02571
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
NINOMIYA YUZO 九州大学, 味覚・嗅覚センサ研究開発センター, 特任教授 (50076048)
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| Co-Investigator(Kenkyū-buntansha) |
重村 憲徳 九州大学, 歯学研究院, 教授 (40336079)
吉田 竜介 九州大学, 歯学研究院, 准教授 (60380705)
實松 敬介 九州大学, 歯学研究院, 助教 (70567502)
岩槻 健 東京農業大学, 応用生物科学部, 准教授 (50332375)
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| Co-Investigator(Renkei-kenkyūsha) |
Yasumatsu Keiko (Nakano Keiko) 九州大学, 味覚・嗅覚センサ研究開発センター, 特任准教授 (50380704)
Takai Shingo 九州大学, 大学院歯学研究院, 助教 (30760475)
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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 |
¥40,820,000 (Direct Cost: ¥31,400,000、Indirect Cost: ¥9,420,000)
Fiscal Year 2017: ¥12,740,000 (Direct Cost: ¥9,800,000、Indirect Cost: ¥2,940,000)
Fiscal Year 2016: ¥14,300,000 (Direct Cost: ¥11,000,000、Indirect Cost: ¥3,300,000)
Fiscal Year 2015: ¥13,780,000 (Direct Cost: ¥10,600,000、Indirect Cost: ¥3,180,000)
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| Keywords | 口腔腸管味覚センサー / 糖輸送体受容経路 / 代謝センサー / 食欲調節ホルモン / レプチン / エンドカンナビノイド / コレシストキニン / 肥満 / 歯学 / 味覚 / シグナル伝達 / 内分泌 / 神経科学 |
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| Outline of Final Research Achievements |
The present study investigated molecular basis of taste perception and humoral modulation of taste/hormone sensing cells in the oral-gut-brain circuit and its role in regulating food intake. The results showed that mouse sweet-sensitive cells in the oral cavity and gut possess at least two sweet reception systems; one is T1R2/T1R3 which can detect not only sugars but also artificial sweeteners and the other is T1Rs-independent sugar sensing system including glucose transporters (SGLTs/GLUTs), a metabolic sensor(KATP) and GLP-1, gut peptide hormone. In addition to GLP-1 for sweet signal transmission, CCK was shown be involved in bitter signal transmission in bitter-responsive cells. Leptin, a satiety hormone, inhibits sweet taste responses and glucose absorption via activation of KATP involved in the sugar sensing pathway of sweet-sensitive cells. This taste modulation by leptin may be involved in regulating energy homeostasis, of which the abnormality may possibly lead to the obesity.
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