| Project/Area Number |
18K16242
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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 54040:Metabolism and endocrinology-related
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
Morita Shuhei 和歌山県立医科大学, 医学部, 講師 (50372868)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2020: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 小胞体ストレス / 小胞体ストレス応答 / 膵β細胞 / 糖尿病 |
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| Outline of Final Research Achievements |
NOD mice reversed diabetes with KIRA8 were maintained reversed state without significant changes of body weight nor health condition. It is suggested that KIRA8 shows some long-term effects on NOD mice. In addition, we reported that nAChR signaling has protective effects against hyper-activation of IRE1α and excessive ER stress, suggesting that it could be one of the factors to affect the effect of KIRA.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、新規発症1型糖尿病モデルマウスにおいて細胞内小器官である小胞体を新規標的とした小分子化合物KIRAの長期効果を示した。また、膵β細胞においてKIRAの働きに影響を及ぼす因子の一つであると考えられるnAChR経路を同定しえた。これらの結果は、治療法の限局した1型糖尿病患者の病態の一旦を示すとともに、新規治療薬としてのKIRAの長期有効性を示唆すると考えられた。
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