Molecular mechanisms in exercise training-induced atheroprotection
| Project/Area Number |
26560404
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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 | Nagoya City University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 動脈硬化 / 運動 / オートファジー / 動脈硬化症 |
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| Outline of Final Research Achievements |
Animal studies have shown that regular exercise prevents atherosclerosis. Autophagy has been functionally linked to homeostasis in organs. Here, we determined if regular exercise-induced autophagy activation is sufficient to mitigate high-fat diet-induced atherosclerosis. Male C57BL/6J mice were randomly assigned into Sedentary (Sed) and (Ex) group. Mice in exercise group were performed voluntary wheel-running exercise for 16 weeks. Mice in both groups were fed 45% high-fat diet. After exercise training periods, aorta tissue was harvested and analyzed autophagy proteins by western blot. We showed that 16 weeks regular exercise prevented high-fat diet-induced obesity and atherosclerosis. Autophagy flux (i.e., LC3-II protein) in Sed mice was greater than Ex mice. These results suggest that exercise training may regulate atherosclerotic plaques formation by autophagy.
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Report
(3 results)
Research Products
(2 results)
