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December 10, 2005AJP Heart and Circulatory Physiology

LV ejection fraction was significantly reduced with HF (49 +/- 6%) compared with sham operated (86 +/- 2%) with no significant differences in ejection fraction among the three infarcted groups.

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Why the study?

Does activation of fatty acid metabolism with fat feeding or a PPARalpha agonist exacerbate LV dysfunction in a rat infarct model of heart failure?

Population

Rats with infarct-induced heart failure (n = 38) or sham-operated rats (n = 10)

Comparison

High-fat diet or PPARalpha agonist fenofibrate… vs Untreated infarcted rats and sham-operated rats

Design

Preclinical

Follow-up

12 weeks

Authors

EMEric E. MorganJRJulie H. RennisonMYMartin E. Young

Discussion

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Overview

Fatty acid activation does not worsen post-infarct LV dysfunction in rats; leaves open relevance to human HF.

Key Points

  • To investigate whether stimulating fatty acid metabolism via high-fat feeding or fenofibrate-induced PPAR-alpha activation increases myocardial lipid accumulation and worsens left ventricular dysfunction in heart failure.
  • Evaluated rats with infarct-induced heart failure (n=38) and sham-operated controls (n=10) over a 12-week intervention period.
  • Assigned infarcted rats to three arms: untreated infarct (n=10), high-fat diet (45% kcal fat, n=15), or the PPAR-alpha agonist fenofibrate (150 mg/kg/day, n=13).
  • Left ventricular ejection fraction dropped significantly following infarction (49 ± 6%) compared with sham controls (86 ± 2%), showing no significant differences among the three infarcted groups.
  • Fenofibrate increased the left ventricular-to-body mass ratio by 24% and upregulated medium chain acyl-CoA dehydrogenase expression and activity without worsening functional or hemodynamic measures.
  • Myocardial ceramide content rose following infarction but did not increase further with a high-fat diet or fenofibrate, whereas myocardial triglyceride increased exclusively in the high-fat diet group.

Structured PICO

Does activation of fatty acid metabolism with fat feeding or a PPARalpha agonist exacerbate LV dysfunction in a rat infarct model of heart failure?

P
Population
Rats with infarct-induced heart failure (n = 38) or sham-operated rats (n = 10)
I
Intervention
High-fat diet (45% kcal fat, n = 15) or PPARalpha agonist fenofibrate (150 mg/kg/day, n = 13) for 12 weeks
C
Comparator
Untreated infarcted rats (n = 10) and sham-operated rats (n = 10)
O
Outcome
Left ventricular (LV) ejection fractionsurrogate

In a rat infarct model of heart failure, upregulation of the fatty acid metabolic pathway via high-fat diet or fenofibrate did not worsen LV dysfunction or dilation.

Cite This Study

Morgan et al. (2005) studied this question.

synapsesocial.com/papers/6a865a52da4bf993812ed761https://doi.org/10.1152/ajpheart.01014.2005
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Also Consider

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