| Project/Area Number |
25670349
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General internal medicine(including psychosomatic medicine)
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| Research Institution | Nagoya University |
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Principal Investigator |
KUZUYA Masahumi 名古屋大学, 未来社会創造機構, 教授 (10283441)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 老化 / 虚弱 / 動物 / サルコぺニア / フレイル / サルコペニア |
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| Outline of Final Research Achievements |
The aim of this study is to develop animal model of frailty that reproduce the symptoms of human frailty. We used SAMP10 as a candidate of the human frailty model. Body weight (BW) of SAMP10 and control SAMR1 mice decreased after 28 weeks old and 36 weeks old, respectively. Compared with SAMR1 mice, spontaneous activity of SAMP10 was lower. Significant decline of grip strength or grip strength/BW was observed in SAMP10 after 28 weeks of age. Endurance capacity of SAMP10 decreased after 16 weeks of age. The significant decline of muscle weight of hindlimb was observed in SAMP10 at 64 weeks compared at 40 weeks of age, and muscle weigh of SAMP10 was significantly lower than those of SAMR1 at the same age. Compared with SAMR1, the levels of mRNA MuRF-1 mRNA were increased in soleus and gastrocnemius of SAMP10, whereas the levels of PGC-1α and IGF-1 mRNAs were decreased in soleus of SAMP10. These results may suggest that SAMP10 is useful model of human frailty.
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