2013 Fiscal Year Final Research Report

Vulnerability of Atrial Fibrillation is Increased in a Rat Model of Metabolic Syndrome Via Phosphorylation of Calcium-Calmodulin-Dependent Protein Kinase II

Research Project

Project/Area Number	24790736
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Circulatory organs internal medicine
Research Institution	University of Tsukuba
Principal Investigator	XU Dong-Zhu 筑波大学, 医学医療系, 助教 (20616651)
Project Period (FY)	2012-04-01 – 2014-03-31
Keywords	心房細動 / 肥満 / リモデリング / Caハンドリング
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.

(1 results)