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2018 Fiscal Year Final Research Report

A study on the mechanism of skeletal muscle atrophy in chronic kidney disease as aging-related sarcopenia

Research Project

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Project/Area Number 16K01828
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Applied health science
Research InstitutionWakayama Medical University

Principal Investigator

SONOU Tomohiro  和歌山県立医科大学, 医学部, 博士研究員 (70614866)

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)
Project Period (FY) 2016-04-01 – 2019-03-31
Keywordsサルコペニア / 慢性腎臓病 / 尿毒素 / 骨格筋
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.

Free Research Field

健康科学

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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Published: 2020-03-30  

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