Departamento de Desportos, Centro de Educação Física e Desportos, UFES-Universidade Federal do Espírito Santo, Vitória, ES.
Arq Bras Cardiol. 2011 Sep;97(3):232-40. doi: 10.1590/s0066-782x2011005000061. Epub 2011 May 13.
Several mechanisms have been proposed to contribute to cardiac dysfunction in obesity models, such as alterations in calcium (Ca²⁺) handling proteins and β-adrenergic receptors. Nevertheless, the role of these factors in the development of myocardial dysfunction induced by obesity is still not clear.
The purpose of this study was to investigate whether obesity induced by hypercaloric diets results in cardiac dysfunction. Furthermore, it was evaluated whether this functional abnormality in obese rats is related to abnormal Ca²⁺ handling and the β-adrenoceptor system.
Male 30-day-old Wistar rats were fed with standard food (C) and a cycle of five hypercaloric diets (Ob) for 15 weeks. Obesity was defined as increases in body fat percentage in rats. Cardiac function was evaluated by isolated analysis of the left ventricle papillary muscle under basal conditions and after inotropic and lusitropic maneuvers.
Compared with the control group, the obese rats had increased body fat and glucose intolerance. The muscles of obese rats developed similar baseline data, but the myocardial responsiveness to post-rest contraction stimulus and increased extracellular Ca²⁺ were compromised. There were no changes in cardiac function between groups after β-adrenergic stimulation.
Obesity promotes cardiac dysfunction related to changes in intracellular Ca²⁺ handling. This functional damage is probably caused by reduced cardiac sarcoplasmic reticulum Ca²⁺ ATPase (SERCA2) activation via Ca²⁺ calmodulin kinase.
已有多种机制被提出以解释肥胖模型中心脏功能障碍的发生，如钙（Ca²⁺）处理蛋白和β-肾上腺素能受体的改变。然而，这些因素在肥胖诱导的心肌功能障碍中的作用仍不清楚。
本研究旨在探讨高热量饮食诱导的肥胖是否会导致心脏功能障碍。此外，还评估了肥胖大鼠的这种功能异常是否与 Ca²⁺处理和β-肾上腺素能受体系统的异常有关。
雄性 30 日龄 Wistar 大鼠分别给予标准饮食（C）和五轮高热量饮食（Ob），共 15 周。肥胖定义为大鼠体脂百分比增加。通过左心室乳头肌的离体分析，在基础条件下和在变力和变时操作后评估心脏功能。
与对照组相比，肥胖组大鼠体脂增加，糖耐量受损。肥胖大鼠的肌肉有相似的基础数据，但心肌对后收缩刺激和增加细胞外 Ca²⁺的反应性受损。β-肾上腺素能刺激后两组之间的心脏功能没有变化。
肥胖导致与细胞内 Ca²⁺处理变化相关的心脏功能障碍。这种功能损伤可能是由于心脏肌浆网 Ca²⁺-ATP 酶（SERCA2）的激活减少所致，其机制可能是 Ca²⁺钙调蛋白激酶的作用。
