| Project/Area Number |
26560407
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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 |
Applied health science
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| Research Institution | University of Marketing and Distribution Sciences |
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Principal Investigator |
Kitamura Hiromi 流通科学大学, 人間社会学部, 准教授 (00360090)
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| Co-Investigator(Kenkyū-buntansha) |
矢野 博己 川崎医療福祉大学, 医療技術学部, 教授 (20248272)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | オートファジー / 自発運動 / 脂肪組織 / 腸内細菌 / TLR5ノックアウトマウス / Firmicutes / LC-3 / ATG5 / ATG7 / LC3 / atg5 / 脂肪滴 |
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| Outline of Final Research Achievements |
In this study, to elucidate the molecular mechanism of exercise on improvement of obesity and related diseases, we studied using TLR5 deficient (KO5) mice.
As results, voluntary exercise for 20 weeks decreased fat mass in epididymal and lipid droplets in liver on KO5 mice. In adipose tissues, the mRNA expressions of Atg5 and Atg7 were significantly enhanced by voluntary exercise, although LC3b mRNA was downregulated. The LC3-Ⅱ/LC3-Ⅰ ratio in adipose tissues attenuated in that of WT mice by voluntary exercise but enhanced in that of KO5 mice. Voluntary exercise decreased microbiota diversity and Firmicutes phylum related to obesity on KO5 mice. However, there were no significant correlations between autophagy-related proteins and Firmicutes or Bacteroidetes phylums.
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