Effects of a High Saturated Fat Diet on Cardiac Hypertrophy and Dysfunction in Response to Pressure Overload

Chess, David J.; Lei, Biao; Hoit, Brian D.; Azimzadeh, Agnes M.; Stanley, William C.

doi:10.1016/j.cardfail.2007.09.004

« Previous Next »Journal of Cardiac Failure
Volume 14, Issue 1 , Pages 82-88, February 2008

Effects of a High Saturated Fat Diet on Cardiac Hypertrophy and Dysfunction in Response to Pressure Overload

David J. Chess, BS
- Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio
Biao Lei, MD, PhD
- Division of Cardiology, Department of Medicine, University of Maryland, Baltimore, Maryland
Brian D. Hoit, MD
- Department of Medicine, School of Medicine, Case Western Reserve University, Cleveland, Ohio
Agnes M. Azimzadeh, PhD
- Department of Surgery, University of Maryland, Baltimore, Maryland
William C. Stanley, PhD
- Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio
- Division of Cardiology, Department of Medicine, University of Maryland, Baltimore, Maryland
- Reprint requests: William C. Stanley, PhD, Division of Cardiology, Department of Medicine, University of Maryland-Baltimore, 20 Penn St., HSF-II, Room S022, Baltimore, MD 21201.

Received 15 May 2007; received in revised form 2 August 2007; accepted 10 September 2007. published online 03 January 2008.

Abstract

Background

Dietary lipid content effects activation of peroxisome proliferator-activated receptor-α (PPAR-α) and may accelerate cardiac hypertrophy and dysfunction in response to pressure overload. This study investigated the effects of a high-fat diet on the development of cardiac hypertrophy.

Methods and Results

C57BL/6J mice (n = 14–16/group) underwent transverse aortic constriction (TAC) or sham surgery and were fed either standard low-fat diet (STD; 10% fat) or a high-fat diet (HFD; 60% fat) for 16 weeks. Sham mice showed no differences between STD and HFD for heart mass or echocardiographic parameters despite greater plasma free fatty acid and leptin concentrations with HFD. TAC increased heart mass and decreased ejection fraction similarly in both groups. Left ventricular end systolic and diastolic diameters with TAC were increased compared with shams on the HFD (P < .05), but were not different from STD TAC mice. High-fat feeding increased expression of PPAR-α–regulated genes. The activity of medium chain acyl-coenzyme A dehydrogenase (MCAD), a marker of fatty acid oxidation capacity, was increased in HFD TAC mice compared with STD, consistent with PPAR-α activation.