Trimetazidine Therapy Prevents Obesity-Induced Cardiomyopathy in Mice

Abstract Obesity is a significant risk factor for the development of cardiovascular disease. Inhibiting fatty acid oxidation has emerged as a novel approach for the treatment of ischemic heart disease. Our aim was to determine whether pharmacologic inhibition of 3-ketoacyl-coenzyme A thiolase (3-KAT...

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Bibliographic Details
Published in:	Canadian journal of cardiology 2014-08, Vol.30 (8), p.940-944
Main Authors:	Ussher, John R., PhD, Fillmore, Natasha, MSc, Keung, Wendy, PhD, Mori, Jun, MD, PhD, Beker, Donna L, Wagg, Cory S, Jaswal, Jagdip S., PhD, Lopaschuk, Gary D., PhD
Format:	Article
Language:	eng
Subjects:	Acetyl-CoA C-Acyltransferase - antagonists & inhibitors Animals Cardiomyopathies - etiology Cardiomyopathies - prevention & control Cardiovascular Echocardiography Heart Ventricles - diagnostic imaging Hypertrophy, Left Ventricular - prevention & control Male Mice Mice, Inbred C57BL Obesity - complications Oxidation-Reduction Palmitates - metabolism Trimetazidine - pharmacology Vasodilator Agents - pharmacology
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Summary:	Abstract Obesity is a significant risk factor for the development of cardiovascular disease. Inhibiting fatty acid oxidation has emerged as a novel approach for the treatment of ischemic heart disease. Our aim was to determine whether pharmacologic inhibition of 3-ketoacyl-coenzyme A thiolase (3-KAT), which catalyzes the final step of fatty acid oxidation, could improve obesity-induced cardiomyopathy. A 3-week treatment with the 3-KAT inhibitor trimetazidine prevented obesity-induced reduction in both systolic and diastolic function. Therefore, targeting cardiac fatty acid oxidation may be a novel therapeutic approach to alleviate the growing burden of obesity-related cardiomyopathy.
ISSN:	0828-282X 1916-7075