2021 Fiscal Year Final Research Report
Generation and phenotyping of mice overexpressing slow contractile phenotype promoting factor for the development of new metabolic syndrome drugs
Project/Area Number |
19K11486
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 59020:Sports sciences-related
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Research Institution | Kindai University |
Principal Investigator |
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Project Period (FY) |
2019-04-01 – 2022-03-31
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Keywords | Vgll2 / 遅筋 / 好気的代謝 / トランスジェニックマウス / ノックアウトマウス |
Outline of Final Research Achievements |
Skeletal muscle consumes so much energy that it accounts for 20% of the total body under sedentary conditions. Focusing on the close relationship between muscle fiber type and metabolic capacity, in this study, I examined whether the expression level of Vgll2, a promoter of slower contractile phenotype, also influences an individual's tolerance to obesity, using genetically engineered mice. First, I generated transgenic mice that overexpress Vgll2 in a muscle-specific manner (Vgll2 Tg) and obtained four strains. Furthermore, I found that the body weight gain rate of normally bred Vgll2 Tg mice was significantly lower than that of wild-type mice. On the other hand, the rate of weight gain of Vgll2-deficient mice (Vgll2 KO) fed a high-fat diet was significantly increased compared to wild-type mice.
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Free Research Field |
筋線維タイプ制御
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Academic Significance and Societal Importance of the Research Achievements |
本研究では、独自に作出したVgll2 KOマウスおよびVgll2 Tgマウスを用いて、Vgll2の発現レベルが個体の肥満しやすさに関係している可能性を示すことに成功した。研究期間内に分子機構の解明までには至らなかったが、Vgll2は骨格筋選択的に発現することから、筋代謝調節を介して、全身の代謝に影響をおよぼしているものと考えられる。運動刺激によって活性化する点を加味すると、Vgll2の制御機構には、人為的に活性操作の可能な、生活習慣病の治療標的となる分子が存在する可能性は高い。
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