Vulnerability of Atrial Fibrillation is Increased in a Rat Model of Metabolic Syndrome Via Phosphorylation of Calcium-Calmodulin-Dependent Protein Kinase II
| Project/Area Number |
24790736
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | University of Tsukuba |
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Principal Investigator |
XU Dong-Zhu 筑波大学, 医学医療系, 助教 (20616651)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 心房細動 / 肥満 / リモデリング / Caハンドリング / カルシウム調節 |
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| Research Abstract |
Metabolic syndrome is associated with the pathogenesis of atrial fibrillation(AF), however, underlying mechanism still remains unkown.To clarify this point, model of metabolic syndrome was made by feeding a rat with high fat diet and AF vulnerability as well as pathophysiological backgraound was evaluated. AF duration was significantly prolonged in high fat diet rats, and western blotting analysis revealed that phosphorylation of calcium-calmodulin-dependent protein kinase II was significantly increased in the left atrial from rats with high fat diet.
High fat diet rats provided similar condition to that of metabolic syndrome, and increased AF vulnerability. Altemation of Ca handling proteins may be involved in the development of arrhythmodenic substrate that could promote AF in metabolic syndrome.
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Report
(3 results)
Research Products
(2 results)
