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Hypercaloric diet models do not develop heart failure, but the excess sucrose promotes contractility dysfunction.
Amanda Martins Matias1, Priscila Murucci Coelho1, Vinícius Bermond Marques2
1Postgraduate Program in Nutrition and Health, Center of Health Sciences, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.
Plos One
|February 8, 2020
Summary
High-fat and high-sucrose diets induced obesity but not heart failure in rats. Excess sucrose impaired cardiomyocyte contractility, independent of obesity.
Area of Science:
- Cardiovascular Physiology
- Nutritional Science
- Obesity Research
Background:
- Obesity is a significant risk factor for cardiac remodeling and heart failure.
- Dietary factors play a crucial role in the development of obesity-related cardiovascular diseases.
Purpose of the Study:
- To develop and characterize an experimental obesity model using hypercaloric diets.
- To investigate the impact of high-sucrose, high-fat, and combined diets on cardiac remodeling and heart failure predisposition.
Main Methods:
- Male Wistar rats were fed control, high-sucrose, high-fat, or high-fat/high-sucrose diets for 20 weeks.
- Evaluated general characteristics, comorbidities, cardiac weights, myocyte size, collagen content, cardiac function, and heart failure markers.
- Assessed cardiomyocyte contractile function and calcium handling.
Main Results:
- High-fat and high-fat/high-sucrose diets successfully induced obesity.
- No significant cardiac remodeling or heart failure signals were observed in any diet group.
- High-sucrose diet alone impaired cardiomyocyte contractility and altered calcium transient amplitude.
Conclusions:
- Hypercaloric diets (high-sucrose, high-fat, or combined) did not induce cardiac remodeling or heart failure in this obesity model.
- Excess sucrose consumption, independent of obesity, can lead to cardiomyocyte contractile dysfunction.
- Further research is needed to understand the specific mechanisms of sucrose-induced myocyte dysfunction.
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