2017 Fiscal Year Final Research Report
The molecular mechanism of sarcopenia associated with male menopause
Project/Area Number |
15K09441
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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 |
Research Field |
Endocrinology
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Research Institution | Kyoto Prefectural University of Medicine |
Principal Investigator |
Fukui Michiaki 京都府立医科大学, 医学(系)研究科(研究院), 教授 (30247829)
|
Co-Investigator(Kenkyū-buntansha) |
山崎 真裕 京都府立医科大学, 医学(系)研究科(研究院), 講師 (50309134)
田中 武兵 京都府立医科大学, 医学(系)研究科(研究院), 助教 (70713717)
濱口 真英 京都府立医科大学, 医学部附属病院, 研究員 (80350883)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | Sarcopenia / Muscle atrophy / Diabetes / Glucose metabolism / Metabolic syndrome / Androgen / Testosterone |
Outline of Final Research Achievements |
Sarcopenia has been thought to be a diabetic complication. Sarcopenia occurs during male menopause, and it is a risk for diabetes. However, the molecular mechanism of sarcopenia caused by reduced androgen signal has not been clarified yet. We established a murine model for male menopause sarcopenia and performed a transcriptome analysis. Scid1 and smox were identified as mRNAs at low expression level in the atrophic soleus muscle. The expression level of mir23b-3p was upregulated in the atrophic muscle. We revealed that mir23b-3p could repress pten and could upregulate muscle protein synthesis.
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Free Research Field |
糖尿病学
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