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Am J Physiol Heart Circ Physiol (December 9, 2005). doi:10.1152/ajpheart.01014.2005
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Submitted on September 23, 2005
Accepted on December 6, 2005

Effects of Chronic Activation of Peroxisome Proliferator Activated Receptor Alpha or High Fat Feeding in a Rat Infarct Model of Heart Failure

Eric E Morgan1, Julie H Rennison1, Martin E Young2, Tracy A McElfresh1, Theodore A Kung1, Kou-Yi Tserng3, Brian D Hoit4, William C Stanley1, and Margaret P Chandler1*

1 Physiology & Biophysics, Case Western Reserve University, Cleveland, OH, USA
2 Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA
3 Veteran Affairs Medical Research Center, Cleveland, OH, USA
4 Department of Medicine, Case Western Reserve University & University Hospitals, Cleveland, OH, USA

* To whom correspondence should be addressed. E-mail: mpc10{at}po.cwru.edu.

Intracardiac accumulation of lipid and related intermediates (e.g. ceramide) is associated with cardiac dysfunction, and may contribute to the progression of heart failure (HF). Over-expression of nuclear receptor peroxisome proliferator activated receptor {alpha} (PPAR{alpha}) increases intramyocellular ceramide and left ventricular (LV) dysfunction. We tested the hypothesis that activation of fatty acid metabolism with fat feeding or a PPAR{alpha} agonist increases myocardial triglyceride and/or ceramide, and exacerbates LV dysfunction in HF. Rats with infarct-induced HF (n=38) or sham rats (Sham n=10) were either untreated (INF, n=10), fed a high fat diet (45% kcal fat, INF+Fat, n=15), or fed the PPAR{alpha} agonist fenofibrate (150 mg.kg-1.day-1, INF+Feno, n=13) for 12 weeks. LV ejection fraction (EF) was significantly reduced with HF (49±6%) compared to Sham (86±2%) with no significant differences in EF (or other functional or hemodynamic measures) among the three infarcted groups. Treatment with the PPAR{alpha} agonist resulted in LV hypertrophy (24% increase in LV/body mass ratio) and induced mRNAs encoding for PPAR{alpha} regulated genes, as well as protein expression and activity of medium chain acyl-CoA dehydrogenase (compared to INF and INF+Fat groups). Myocardial ceramide content was elevated in the INF group compared to sham rats, with no further change in the INF+Fat or INF+Feno groups. Myocardial triglyceride was unaffected by infarction but increased in the INF+Fat group. In conclusion, LV dysfunction and dilation are not worsened despite up-regulation of the fatty acid metabolic pathway and LV hypertrophy or accumulation of myocardial triglyceride in the rat infarct model of HF.




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