Mechanism of obesity in female CRTC1 Knockout mice
| Project/Area Number |
18K19174
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Review Section |
Medium-sized Section 38:Agricultural chemistry and related fields
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
佐々木 勉 大阪大学, 医学系研究科, 寄附講座准教授 (20534879)
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| Project Period (FY) |
2018-06-29 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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| Keywords | 肥満 / 高脂肪食 / 転写因子 |
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| Outline of Final Research Achievements |
Previously, we found that the deficiency of CREB coactivator CRTC1 accelerated high-fat diet induced obesity in female mice. In general, an increase in food intake and decrease in energy expenditure causes obesity. Thus, we checked these factors in female CRTC1 knockout mice. We found that female CRTC1 KO mice consumed more high-fat diet than wild type animals.However, there was no change in energy expenditure between CRTC1 knockout mice and wild type mice. Next, we investigated the gene expression that relates to food intake regulation in hypothalamus. We found that MC4R was increased in the hypothalamus of CRTC1KO mice. In conclusion, we found that CRTC1 may act on hypothalamus regulating food intake.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究により転写補因子であるCRTC1が肥満遺伝子のひとつであるMC4Rの下流に存在し、遺伝子発現調節を行うことにより、摂食を調節していることが示唆された。また、CRTC1欠損にともなう摂食量の増加はオスよりもメスの方が顕著であることから、CRTC1は女性における摂食調節に関与する因子であると推測される。これまでに女性の肥満に関する遺伝的因子はほとんど報告されておらず、女性に特化した肥満治療薬はあまりない。このため、CRTC1の活性化が女性における肥満治療の新たな標的分子になりうると期待される。
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Report
(4 results)
Research Products
(5 results)
