Postgraduate Program in Nutrition and Health, Center of Health Sciences, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.
Center of Health Sciences, Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.
PLoS One. 2020 Feb 7;15(2):e0228860. doi: 10.1371/journal.pone.0228860. eCollection 2020.
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+.
几种疾病与脂肪组织过多有关，肥胖被认为是心脏重构和心力衰竭发展的独立危险因素。人们已经研究了饮食方面，以阐明这些过程中涉及的机制。因此，目的是开发和表征一种来自高热量饮食的肥胖实验模型，该模型导致心脏重构和易患心力衰竭。30 日龄雄性 Wistar 大鼠（n = 52）随机分为 4 组：对照组（C）、高蔗糖（HS）、高脂肪（HF）和高脂肪高蔗糖（HFHS），共 20 周。评估一般特征、合并症、心脏、左心室（LV）和右心室、心房重量以及与胫骨长度的关系。测量 LV 心肌细胞横截面积和间质胶原分数。通过血流动力学分析和心肌细胞收缩功能测定评估心脏功能。通过肺充血、右心室肥厚和血流动力学参数分析心力衰竭。HF 和 HFHS 模型通过增加肥胖指数（C = 8.3 ± 0.2%对 HF = 10.9 ± 0.5%，HFHS = 10.2 ± 0.3%）导致肥胖。形态参数和心力衰竭信号没有变化。HF 和 HFHS 导致舒张 50%时间缩短，而没有心肌细胞收缩损伤。HS 模型表现出心肌细胞收缩功能障碍，缩短率降低（C：8.34 ± 0.32%对 HS：6.91 ± 0.28%），Ca2+瞬变幅度也高于 HFHS。总之，基于大量糖、猪油或两者组合的实验饮食在肥胖或过量蔗糖的情况下并没有促进心脏重构和易患心力衰竭。然而，过量的蔗糖会导致心肌细胞收缩功能障碍，同时改变心肌细胞对细胞内 Ca2+的敏感性。
