Alterations in glucose and fatty acid metabolism are believed to contribute to the development of heart failure. Peroxisome Proliferator Activated Receptor α (PPARα) is a transcription factor that regulates fatty acid metabolism and is frequently reported to be reduced in heart failure. However, it is controversial whether this decline in PPARα mediates the development of cardiac hypertrophy and heart failure. To improve our understanding of the role of cardiac PPARα we generated a tamoxifen inducible cardiac-specific PPARα knockout mouse (cPPAR
-/-
). Control (Mer-Cre-Mer and Flox
-/-
) mice and cPPAR
-/-
(Mer-Cre-Mer and Flox
+/+
) mice were treated with tamoxifen at ~2.5 months and were studied 5 weeks after treatment. We verified loss of cardiac PPARα using western blot. cPPAR
-/-
mice appear healthy with normal body weight gain and survival. To examine the impact of cardiac deletion of PPARα on cardiac function we performed echocardiography on control and cPPAR
-/-
. There was no reduction in systolic function between control and cPPAR
-/-
mice. Ejection fraction (Control, 56.3±0.9; cPPAR
-/-
, 59.7±0.1) and fractional shortening (Control, 29.1±0.5; cPPAR
-/-
, 31.5±0.1) were similar in cPPAR
-/-
compared to control hearts. Interestingly however, baseline heart rate was significantly lower in cPPAR
-/-
versus control mice (Control, 531.3±18.3; cPPAR
-/-
, 459.8±2.9 bpm). In addition to having normal cardiac function, heart weights were similar between control and cPPAR
-/-
mice. Overall, these data indicate that an acute reduction in myocardial PPARα per se does not cause cardiac dysfunction. However these data do not exclude the possibility that loss of PPARα could drive cardiac pathology in the context of other signals.
Effects of Exercise Training on Myocardial Fatty Acid Metabolism in Rats With Depressed Cardiac Function Induced by Transient Ischemia
