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A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
Published on: December 2, 2016
Low-carbohydrate/high-fat diet attenuates pressure overload-induced ventricular remodeling and dysfunction
Monika K Duda1, Karen M O'Shea, Biao Lei
1Division of Cardiology, Department of Medicine, University of Maryland, Baltimore, Maryland 21201, USA.
Journal of Cardiac Failure
|May 14, 2008
Summary
A low-carbohydrate/high-fat diet prevented left ventricular (LV) remodeling and dysfunction from pressure overload in rats. This diet lowered insulin and leptin, key factors in cardiac growth.
Area of Science:
- Cardiology
- Nutritional Science
- Physiology
Background:
- The impact of dietary carbohydrate and fat on left ventricular (LV) hypertrophy and contractile dysfunction due to pressure overload is unclear.
- High-carbohydrate diets may exacerbate cardiac remodeling under stress.
Purpose of the Study:
- To investigate the effects of low-carbohydrate/high-fat versus high-carbohydrate diets on pressure overload-induced cardiac remodeling.
- To test the hypothesis that a low-carbohydrate/high-fat diet protects against LV hypertrophy and dysfunction.
Main Methods:
- Rats were assigned to high-carbohydrate (starch or sucrose) or low-carbohydrate/high-fat diets.
- Abdominal aortic banding (AAB) was performed to induce pressure overload for 2 months.
- Cardiac mass, volumes, gene expression, and hormonal levels were assessed.
Main Results:
- All diets led to increased LV mass after AAB.
- High-carbohydrate diets promoted LV dilation and altered myosin heavy chain mRNA ratios.
- The low-carbohydrate/high-fat diet group showed attenuated LV remodeling, with lower insulin and leptin levels.
Conclusions:
- A low-carbohydrate/high-fat diet mitigated pressure overload-induced LV remodeling compared to high-carbohydrate diets.
- Lower circulating insulin and leptin concentrations may mediate the protective effects of the low-carbohydrate/high-fat diet.
- Insulin and leptin may play a role in the development of LV hypertrophy and dysfunction under pressure overload.
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