| Project/Area Number |
18K14417
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 38050:Food sciences-related
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| Research Institution | Kansai University of Welfare Sciences (2020-2022)
Kagoshima Women's Junior College (2019)
Utsunomiya University (2018) |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 嗜好性 / 食脂肪 / PI3K/Akt-mTORシグナル伝達経路 / PI3K/Akt-mTOR / PI3K pathway / 油脂 |
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| Outline of Final Research Achievements |
We revealed that ingestion of dietary fat increased activation of phosphatidylinositol 3-kinase (PI3K)/Akt-mammalian target of Rapamycin (mTOR) signaling pathway in the neurons in the hippocampus in mice by animal behavioral studies. Additionally, we examined the activation of the hippocampal PI3K-Akt-mTOR signaling pathway during ingestion of dietary fat is mediated via the mu-opioid system and that mu-opioid receptors in the hippocampus are involved in the palatability. These results indicated the PI3K/Akt-mTOR signaling pathway in the hippocampal neurons participates in the palatability of dietary fat via mu-opioid receptors in the hippocampus.
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| Academic Significance and Societal Importance of the Research Achievements |
脂肪を多く含む食品は、我々人間や動物をやみつきにさせる高い嗜好性を持っている。その一方で、食脂肪の過剰摂取は生活習慣病のリスクファクターである肥満を引き起こすことから問題視されている。本研究により、海馬神経細胞のPI3K/Akt-mTORシグナル伝達経路は、食脂肪の嗜好性の発現に関与していることが示唆され、高脂肪食品に対する高度な嗜好性の形成・維持のメカニズムの一端が明らかとなった。今後、高脂肪食品の嗜好性のメカニズムがより詳細に明らかとなれば、高嗜好性かつ低カロリーの油脂代替物の開発に応用が可能であると期待される。
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