Carvajal Karla, Balderas-Villalobos Jaime, Bello-Sanchez Ma Dolores, Phillips-Farfán Bryan, Molina-Muñoz Tzindilu, Aldana-Quintero Hugo, Gómez-Viquez Norma L
Laboratorio de Nutrición Experimental, Instituto Nacional de Pediatría, Mexico City, Mexico.
Laboratorio de Nutrición Experimental, Instituto Nacional de Pediatría, Mexico City, Mexico; Departamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados-Instituto Politécnico Nacional, Mexico City, Mexico.
Cell Calcium. 2014 Nov;56(5):408-15. doi: 10.1016/j.ceca.2014.08.003. Epub 2014 Aug 10.
Obesity and insulin resistance (IR) are strongly connected to the development of subclinical cardiac dysfunction and eventually can lead to heart failure, which is the main cause of morbidity and death in patients having these metabolic diseases. It has been considered that excessive fat tissue may play a critical role in producing systemic IR and enhancing reactive oxygen species (ROS) generation. This oxidative stress (OS) may elicit or exacerbate IR. On the other hand, evidence suggests that some of the cellular mechanisms involved in the pathophysiology of obesity and IR-related cardiomyopathy are excessive myocardial ROS production and abnormal Ca(2+) homeostasis. In addition, emerging evidence suggests that augmented ROS production may contribute to Ca(2+) mishandling by affecting the redox state of key proteins implicated in this process. In this review, we focus on the role of Ca(2+) mishandling in the development of cardiac dysfunction in obesity and IR and address the evidence suggesting that OS might also contribute to cardiac dysfunction by affecting Ca(2+) handling.
肥胖与胰岛素抵抗（IR）与亚临床心脏功能障碍的发生密切相关，最终可能导致心力衰竭，而心力衰竭是患有这些代谢性疾病患者发病和死亡的主要原因。人们认为，过多的脂肪组织可能在产生全身性IR和增强活性氧（ROS）生成方面起关键作用。这种氧化应激（OS）可能引发或加剧IR。另一方面，有证据表明，肥胖和IR相关心肌病病理生理学中涉及的一些细胞机制是心肌ROS产生过多和钙（Ca2+）稳态异常。此外，新出现的证据表明，ROS生成增加可能通过影响参与该过程的关键蛋白质的氧化还原状态而导致Ca2+处理不当。在本综述中，我们重点关注Ca2+处理不当在肥胖和IR患者心脏功能障碍发展中的作用，并探讨有证据表明OS也可能通过影响Ca2+处理而导致心脏功能障碍。
