Gonçalves Nádia, Silva Ana Filipa, Rodrigues Patrícia Gonçalves, Correia Eugénia, Moura Cláudia, Eloy Catarina, Roncon-Albuquerque Roberto, Falcão-Pires Inês, Leite-Moreira Adelino F
Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal;
Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal; Department of Paediatric Cardiology, Centro Hospitalar São João, Porto, Portugal;
Am J Physiol Heart Circ Physiol. 2016 Mar 15;310(6):H655-66. doi: 10.1152/ajpheart.00684.2015. Epub 2016 Jan 22.
"Obesity cardiomyopathy" effects have been widely described; however, the specific contribution of metabolic changes and altered adipokine secretion are still uncharacterized. Moreover, a diagnosis based on body mass index might not be the most accurate to identify increased adiposity and its outcomes. In this study, we aimed to determine the impact of a Western-type diet [hypercaloric diet (HCD)] ingestion on biventricular structure and function, as well as the metabolic and endocrine changes that occur before the establishment of overt obesity. Wistar rats were fed for 6 wk with a regular diet or HCD. At the end of the protocol, metabolic tests, cardiac structure, and functional evaluation were performed, and blood and tissue samples collected to perform histological, molecular biology, and functional studies. The animals that ingested the HCD presented increased adiposity and larger adipocyte cross-sectional area, but similar body weight compared with the regular diet group. At the cardiac level, HCD induced biventricular cardiomyocyte hypertrophy, fibrosis, increased stiffness, and impaired relaxation. Galectin-3 plasma expression was likewise elevated in the same animals. The nutritional modulation also altered the secretory pattern of the adipose tissue, originating a proinflammatory systemic environment. In this study, we observed that before "clinical" overweight or frank obesity is established, the ingestion of a HCD-induced cardiac remodeling manifests by increased biventricular stiffness and diastolic dysfunction. The mechanism triggering the cardiac alterations appears to be the proinflammatory environment promoted by the adipose tissue dysfunction. Furthermore, galectin-3, a profibrotic molecule, might be a potential biomarker for the myocardial alterations promoted by the HCD before overweight or obesity.
“肥胖性心肌病”的影响已得到广泛描述；然而，代谢变化和脂肪因子分泌改变的具体作用仍未明确。此外，基于体重指数的诊断可能并非识别肥胖增加及其后果的最准确方法。在本研究中，我们旨在确定西式饮食[高热量饮食（HCD）]摄入对双心室结构和功能的影响，以及在明显肥胖形成之前发生的代谢和内分泌变化。将Wistar大鼠用常规饮食或HCD喂养6周。在实验方案结束时，进行代谢测试、心脏结构和功能评估，并采集血液和组织样本以进行组织学、分子生物学和功能研究。摄入HCD的动物与常规饮食组相比，肥胖增加且脂肪细胞横截面积更大，但体重相似。在心脏水平，HCD诱导双心室心肌细胞肥大、纤维化、僵硬度增加和舒张功能受损。同样，在这些动物中半乳糖凝集素-3的血浆表达也升高。营养调节还改变了脂肪组织的分泌模式，产生了促炎的全身环境。在本研究中，我们观察到在“临床”超重或明显肥胖形成之前，摄入HCD诱导的心脏重塑表现为双心室僵硬度增加和舒张功能障碍。引发心脏改变的机制似乎是脂肪组织功能障碍所促进的促炎环境。此外，半乳糖凝集素-3，一种促纤维化分子，可能是HCD在超重或肥胖之前促进心肌改变的潜在生物标志物。
