Molecular physiological basis of modulation and repair by oxidative stress in oral/gut/ brain chemosensory-endocrine interaction for dietary regulation.
| Project/Area Number |
18H02968
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 57010:Oral biological science-related
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| Research Institution | Kyushu University |
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Principal Investigator |
Ninomiya Yuzo 九州大学, 五感応用デバイス研究開発センター, 特任教授 (50076048)
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| Co-Investigator(Kenkyū-buntansha) |
吉田 竜介 岡山大学, 医歯薬学総合研究科, 教授 (60380705)
岩田 周介 九州大学, 歯学研究院, 助教 (60780062)
安松 啓子 九州大学, 五感応用デバイス研究開発センター, 特任准教授 (50380704)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2020: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2019: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2018: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | 酸化ストレス / 味覚 / シグナル伝達 / 内分泌 / 神経科学 |
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| Outline of Final Research Achievements |
Leptin and angiotensin II are hormones that regulate eating and drinking cravings in the brain, and sweet and salt taste sensitivities in the peripheral taste organ and contribute to energy and Na+ homeostasis. Also, the hormones at high concentrations are known to act as oxidative stress inducers in their target organs. This study investigated potential effects of oxidative stress on taste cells and target molecules based on analyses of mouse neural and behavioral taste responses and molecular expression. The results showed that oxidative stress agents increased sweet responses and decreased sodium responses and their targets of oxidative stress may be at intracellular region of KATP (sweet taste) known as a leptin target, and at extracellular region of ENaCs (sodium taste) known as an angiotensin II target.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、肥満・高血圧者増加の一因を成す甘味・塩味感受性のレプチン、アンギオテンシンII内分泌調節系の酸化ストレスによる変調について、マウス味神経・行動応答と味細胞の遺伝子・分子発現を基に検索した。その結果、内分泌系が高濃度で誘導する酸化ストレスは、代謝センサー(KATP)発現味細胞を介して甘味上昇を、Naセンサー(ENaC)発現細胞を介して塩味低下を導き、摂取を促進させることを見出した。この酸化ストレスによる甘味塩味感受性・摂取行動変化の発見は、味高嗜好性形成原理の一端を明らかにし、食の健全化への今後の新たな研究展開への起点となり、学際的意義のみならず社会的意義をもたらすものと思われる。
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Report
(4 results)
Research Products
(63 results)
