| Project/Area Number |
21590320
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Fujita Health University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKATANI Masashi 藤田保健衛生大学, 総合医科学研究所, 助教 (00421264)
HITACHI Keisuke 藤田保健衛生大学, 総合医科学研究所, 助教 (10508469)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | マイオスタチン / ホリスタチン / 筋・脂肪 / 脂肪肝 / マイクロRNA / 間葉系細胞 / 骨格筋 / 脂肪組織 / 臓器間クロストーク / miRNA / アクチビン / 筋分化 / 間葉系細胞分化 / フォリスタチン / 骨格筋形成 / 脂肪細胞 / 脂肪肝抑制 / 難治性筋疾患 |
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| Research Abstract |
Myostatin, one of the TGF-β superfamily member, regulates skeletal muscle mass. It also regulates adipose tissue mass and homeostasis. We have devised the method to block myostatin function, and developed hypermuscular transgenic mice. By using the model, we have shown that adipose tissue in myostatin inhibited mice did not show hypertrophy due to increased numbers of mitochondria. Fatty liver induced by high fat diet feeding was prevented by myostatin inhibition, primarily due to blockade of myostatin signaling in skeletal muscle. Fatty acid composition in liver by high fat diet was different between wildtype and myostatin inhibited mice. We also discovered that expression of several miRNAs is altered by myostatin stimulaton and/or inhibition, which could be responsible for actions of myostatin in regulating muscle homeostasis and dynamics of adipocyte growth and turnover.
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