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High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction.

Julie H Rennison1, Tracy A McElfresh, Isidore C Okere

  • 1Dept of Physiology and Biophysics, School of Medicine E558, Case Western Reserve Univ, Cleveland, OH 44106-4970, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|November 23, 2006
PubMed
Summary

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High saturated fat diets did not worsen heart failure progression in rats. Despite increased myocardial ceramide, mitochondrial function and electron transport chain activities improved, preserving cardiac contractility.

Area of Science:

  • Cardiovascular Physiology
  • Metabolic Disorders
  • Mitochondrial Biology

Background:

  • Lipid accumulation in non-fatty tissues contributes to heart failure, obesity, and diabetes.
  • Myocardial lipid accumulation, particularly ceramide, impairs cardiac contractile function and mitochondrial activity.

Purpose of the Study:

  • To investigate if elevated myocardial lipids and ceramide exacerbate heart failure progression.
  • To determine the impact of high saturated fat intake on cardiac function and mitochondrial oxidative phosphorylation in heart failure.

Main Methods:

  • Heart failure (HF) induced by coronary artery ligation in rats.
  • Rats fed either a normal or high saturated fat diet post-ligation.
  • Echocardiography, catheterization, and mitochondrial isolation to assess cardiac function and bioenergetics.

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Main Results:

  • HF rats showed impaired left ventricular (LV) function and remodeling.
  • High saturated fat diet (HF + Sat) did not further impair LV function compared to HF.
  • HF + Sat rats exhibited increased mitochondrial state 3 respiration and elevated electron transport chain (ETC) complex II and IV activities despite higher myocardial ceramide.

Conclusions:

  • High saturated fat intake following coronary artery ligation does not exacerbate heart failure progression.
  • Increased myocardial ceramide in HF + Sat rats was not associated with further cardiac dysfunction.
  • Elevated saturated fat intake may enhance mitochondrial oxidative phosphorylation and ETC activity in the failing heart.