| Project/Area Number |
16K01828
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Applied health science
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
SONOU Tomohiro 和歌山県立医科大学, 医学部, 博士研究員 (70614866)
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| Co-Investigator(Kenkyū-buntansha) |
重松 隆 和歌山県立医科大学, 医学部, 教授 (30187348)
大矢 昌樹 和歌山県立医科大学, 医学部, 講師 (90550301)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | サルコペニア / 慢性腎臓病 / 尿毒素 / 骨格筋 / 腎機能障害 |
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| Outline of Final Research Achievements |
We examined the effect of mineral metabolism disorders with chronic kidney disease (CKD) on skeletal muscle atrophy (sarcopenia), using in vivo and in vitro study. Our in vivo study, we adopted animal CKD model induced hyperparathyroidism in 5/6 nephrectomized (Nx) rats. In spite of a relatively short period (only 4 weeks), rats fed high-phosphate and low-calcium diet in the Nx group were almost observed cachexia in CKD. This result might suggest this model was a useful tool to investigate sarcopenia associated with CKD. In vitro study, we examined myotubes differentiated from rat L6 myoblasts were harvested in DMEM containing 2% horse serum with/without uremic toxins such as Indole-3-acetic acid (IAA) or Indoxyl sulfate (IS). These experiments were implemented in both normal- and high-phosphate conditions. These results might suggest uremic toxins using the present study cannot dramatically harm myotubes and phosphate control is crucial to prevent sarcopenia in CKD.
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| Academic Significance and Societal Importance of the Research Achievements |
骨格筋量と生命予後の関係性が様々な状態で報告されてきており、骨格筋量を維持・増加させるためにも、サルコペニアのメカニズムを明らかにすることは重要である。本研究では、老化現象の一つとしての腎機能の低下に着目し、腎機能低下(慢性腎臓病)モデルを利用することで、サルコペニア研究の比較的短期間での実験手法を提示することができた。また、今回採用した尿毒素は骨格筋に対する直接的な影響を認めなかったが、高リン状態が筋萎縮を誘導したことから腎機能低下による液性因子がサルコペニアの一因であることが明らかになり、今後のサルコペニア研究に対する有用な知見を得ることができた。
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