Role of If channel remodeling in atrial fibrillation appearance in diabets
Project/Area Number |
23790249
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
General physiology
|
Research Institution | Oita University |
Principal Investigator |
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 洞房結節 / 心房細動 / 糖尿病 / 洞不全症候群 / インスリン抵抗性 / Leptin / Atrial fibrillation / Atrial fibrosis |
Research Abstract |
Both the membrane clock and the Ca2+ clock are important in the initiation of the heart beat, and malfunction of these two clocks leads to sinoatrial node (SAN) dysfunction. SAN function and arrhythmic events were evaluated in 14 weeks old male hereditary insulin-resistant Otsuka Long-Evans Tokushima fatty (OLETF) rats and control Long-Evans Tokushima Otsuka (LETO) rats. OLETF rats showed longer correct sinus node recovery time. The mRNA levels of HCN4, RyR2, and phospholamban were downregulated in OLETF rats compared with LETO rats (p<0.01). SAN dysfunction in insulin-resistant rats was associated with malfunction of both membrane clock and Ca clock.
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Report
(4 results)
Research Products
(13 results)