Trimetazidine therapy prevents obesity-induced cardiomyopathy in mice

Can J Cardiol. 2014 Aug;30(8):940-4. doi: 10.1016/j.cjca.2014.04.023. Epub 2014 Apr 29.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetyl-CoA C-Acyltransferase / antagonists & inhibitors
  • Animals
  • Cardiomyopathies / etiology
  • Cardiomyopathies / prevention & control*
  • 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*

Substances

  • Palmitates
  • Vasodilator Agents
  • Acetyl-CoA C-Acyltransferase
  • Trimetazidine