Key result
High-sucrose diet impairs cardiomyocyte contractility, lowering fractional shortening by an absolute ~1.4% without causing remodeling.
Why the study?
Obesity is an independent risk factor for cardiac remodeling and heart failure, prompting the development and characterization of an experimental obesity model from hypercaloric diets resulting in these outcomes.
Do hypercaloric diets promote cardiac remodeling and predisposition to heart failure in a rat model?
Do hypercaloric diets promote cardiac remodeling and predisposition to heart failure in a rat model?
Absolute Event Rate: 6.91% vs 8.34%
p-value: p=<0.05
Hypercaloric diets induced obesity but did not lead to macroscopic heart failure in this rat model, although excess sucrose independently impaired microscopic cardiomyocyte contractility.
Hypercaloric diets without HF remodeling in rats; leaves open sucrose-specific cardiomyocyte dysfunction for translational studies.
Several diseases are associated with excess of adipose tissue, and obesity is considered an independent risk factor for the development of cardiac remodeling and heart failure. Dietary aspects have been studied to elucidate the mechanisms involved in these processes. Thus, the purpose was the development and characterization of an obesity experimental model from hypercaloric diets, which resulted in cardiac remodeling and predisposition to heart failure. Thirty- day-old male Wistar rats (n = 52) were randomized into four groups: control (C), high sucrose (HS), high-fat (HF) and high-fat and sucrose (HFHS) for 20 weeks. General characteristics, comorbidities, weights of the heart, left (LV) and right ventricles, atrium, and relationships with the tibia length were evaluated. The LV myocyte cross sectional area and fraction of interstitial collagen were assayed. Cardiac function was determined by hemodynamic analysis and the contractility by cardiomyocyte contractile function. Heart failure was analyzed by pulmonary congestion, right ventricular hypertrophy, and hemodynamic parameters. HF and HFHS models led to obesity by increase in adiposity index (C = 8.3 ± 0.2% vs. HF = 10.9 ± 0.5%, HFHS = 10.2 ± 0.3%). There was no change in the morphological parameters and heart failure signals. HF and HFHS caused a reduction in times to 50% relaxation without cardiomyocyte contractile damage. The HS model presented cardiomyocyte contractile dysfunction visualized by lower shortening (C: 8.34 ± 0.32% vs. HS: 6.91 ± 0.28), as well as the Ca2+ transient amplitude was also increased when compared to HFHS. In conclusion, the experimental diets based on high amounts of sugar, lard or a combination of both did not promote cardiac remodeling with predisposition to heart failure under conditions of obesity or excess sucrose. Nevertheless, excess sucrose causes cardiomyocyte contractility dysfunction associated with alterations in the myocyte sensitivity to intracellular Ca2+.
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Matias et al. (2020) studied Obesity, cardiac remodeling, and heart failure (n=52). Hypercaloric diets (high-sucrose, high-fat, or high-fat and high-sucrose) vs. Control diet was evaluated on Cardiomyocyte fractional shortening (p=<0.05). Hypercaloric diets did not promote cardiac remodeling with predisposition to heart failure, but excess sucrose caused cardiomyocyte contractility dysfunction with lower fractional shortening (6.91% vs 8.34% in controls).
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