The pathogenesis of sarcopenia induced by abnormal lipid metabolism in chronic kidney disease
| Project/Area Number |
17K19910
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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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| Research Field |
Health science and related fields
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| Research Institution | The University of Tokushima |
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Principal Investigator |
MASUDA Masashi 徳島大学, 大学院医歯薬学研究部(医学域), 助教 (50754488)
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| Co-Investigator(Kenkyū-buntansha) |
竹谷 豊 徳島大学, 大学院医歯薬学研究部(医学域), 教授 (30263825)
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| Research Collaborator |
NIIDA yuki
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| Project Period (FY) |
2017-06-30 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2018: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 脂質代謝異常 / 慢性腎臓病 / 筋萎縮 |
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| Outline of Final Research Achievements |
In this study, we investigated the pathogenesis of muscle atrophy in chronic kidney disease. First, we found out that CKD model rats had decreased stearoyl-CoA desaturase (SCD) gene expression in muscle gastrocnemius. Next, the treatment CKD model mice with unsaturated fatty acids, oleate, exhibited slight improvements of impaired grip strength in CKD rats. In addition, oleate ameliorated upregulation of muscle atrophy relative genes expression and autophagy impairment induced by SCD inhibitor. Taken together, these results suggested that abnormal lipid metabolism in myocyte may provoke muscle atrophy through autophagy impairment in CKD.
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| Academic Significance and Societal Importance of the Research Achievements |
慢性腎臓病（CKD）が悪化して発症する筋萎縮に関する基礎研究の実験系は確立されておらず、発症メカニズム等を理解するために必要な基礎的なデータが圧倒的に足りないのが現状である。しかしながら、本研究成果からCKDの骨格筋で起きる脂質代謝異常がオートファジー障害等の筋分解機構を亢進して筋萎縮を誘発する可能性が示唆されたことは、発展途上の筋萎縮研究分野の大きな飛躍の第一歩となると確信している。また、世界的に急速に高齢化を迎える中、健康寿命の延伸は喫緊の課題であるため、老化に伴う筋萎縮発症機序の新しい発見にもつながれば、現代人や次の世代の人々が抱える大きな問題解決に貢献できる可能性がある。
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Report
(3 results)
Research Products
(6 results)
