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Updated: Jul 19, 2026

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
Published on: December 2, 2016
Low carbohydrate/high-fat diet attenuates cardiac hypertrophy, remodeling, and altered gene expression in
Isidore C Okere1, Martin E Young, Tracy A McElfresh
1Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH 44106-4970, USA.
Insights
High-fat diets may protect against hypertension-induced heart changes. Increased dietary lipids reduced cardiac growth, remodeling, and dysfunction in rats, suggesting a protective effect against cardiovascular stress.
Area of Science:
- Cardiovascular Physiology
- Nutritional Science
- Molecular Biology
Background:
- The impact of dietary fat on cardiac remodeling during hypertension remains unclear.
- Hypertension commonly leads to left ventricular hypertrophy and dysfunction.
Purpose of the Study:
- To investigate how high-fat versus low-fat diets affect left ventricular hypertrophy and remodeling in response to hypertension.
- To assess the influence of diet on molecular markers and contractile function in hypertensive hearts.
Main Methods:
- Dahl salt-sensitive rats were fed low-fat (10%) or high-fat (60%) diets with low or high salt for 12 weeks.
- Cardiac structure, function, and molecular markers (e.g., atrial natriuretic factor mRNA) were analyzed.
- Mitochondrial enzyme activities (citrate synthase, acyl-coenzyme A dehydrogenase) were measured.
Main Results:
- High-salt feeding induced similar hypertension (approx. 190 mm Hg) in both diet groups.
- Low-fat diet exacerbated hypertension-induced left ventricular hypertrophy, reduced ejection fraction, and increased cardiac remodeling markers.
- High-fat diet significantly attenuated these adverse cardiac effects, including molecular alterations and mitochondrial dysfunction.
Conclusions:
- Increased dietary lipid intake mitigates cardiac hypertrophy, remodeling, and contractile dysfunction caused by hypertension.
- Dietary fat composition plays a crucial role in modulating the cardiac response to hypertensive stimuli.
- High-fat feeding may offer a protective strategy against hypertensive heart disease progression.
Abstract:
The effects of dietary fat intake on the development of left ventricular hypertrophy and accompanying structural and molecular remodeling in response to hypertension are not understood. The present study compared the effects of a high-fat versus a low-fat diet on development of left ventricular hypertrophy, remodeling, contractile dysfunction, and induction of molecular markers of hypertrophy (ie, expression of mRNA for atrial natriuretic factor and myosin heavy chain beta). Dahl salt-sensitive rats were fed either a low-fat (10% of total energy from fat) or a high-fat (60% of total energy from fat) diet on either low-salt or high-salt (6% NaCl) chow for 12 weeks. Hearts were analyzed for mRNA markers of ventricular remodeling and activities of the mitochondrial enzymes citrate synthase and medium chain acyl-coenzyme A dehydrogenase. Similar levels of hypertension were achieved with high-salt feeding in both diet groups (systolic pressure of approximately 190 mm Hg). In hypertensive rats fed low-fat chow, left ventricular mass, myocyte cross-sectional area, and end-diastolic volume were increased, and ejection fraction was decreased; however, these effects were not observed with the high-fat diet. Hypertensive animals on low-fat chow had increased atrial natriuretic factor mRNA, myosin heavy chain isoform switching (alpha to beta), and decreased activity of citrate synthase and medium chain acyl-coenzyme A dehydrogenase, which were all attenuated by high-fat feeding. In conclusion, increased dietary lipid intake can reduce cardiac growth, left ventricular remodeling, contractile dysfunction, and alterations in gene expression in response to hypertension.
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