Department of Molecular Biology, Instituto Nacional de Cardiología, Mexico City, Mexico.
Endocrinology, Instituto Nacional de Cardiología, Mexico City, Mexico.
Arch Med Res. 2015 Jul;46(5):392-407. doi: 10.1016/j.arcmed.2015.05.007. Epub 2015 May 23.
Metabolic syndrome (MetS) should be considered a clinical entity when its different symptoms share a common etiology: obesity/insulin resistance as a result of a multi-organ dysfunction. The main interest in treating MetS as a clinical entity is that the addition of its components drastically increases the risk of atherosclerosis. In MetS, the adipose tissue plays a central role along with an unbalanced gut microbiome, which has become relevant in recent years. Once visceral adipose tissue (VAT) increases, dyslipidemia and endothelial dysfunction follow as additive risk factors. However, when the nonalcoholic fatty liver is present, risk of a cardiovascular event is highly augmented. Epicardial adipose tissue (EAT) seems to increase simultaneously with the VAT. In this context, the former may play a more important role in the development of the atherosclerotic plaque than the latter. Hence, EAT may act as a paracrine tissue vis-à-vis the coronary arteries favoring the local inflammation and the atheroma calcification.
代谢综合征(MetS)应被视为一种临床实体,当其不同症状具有共同的病因时:肥胖/胰岛素抵抗是多器官功能障碍的结果。将 MetS 作为一种临床实体进行治疗的主要兴趣在于,其成分的增加极大地增加了动脉粥样硬化的风险。在 MetS 中,脂肪组织与失衡的肠道微生物组一起发挥核心作用,近年来这一点变得越来越重要。一旦内脏脂肪组织(VAT)增加,血脂异常和内皮功能障碍就会成为附加的危险因素。然而,当存在非酒精性脂肪肝时,心血管事件的风险会大大增加。心外膜脂肪组织(EAT)似乎与 VAT 同时增加。在这种情况下,前者在动脉粥样硬化斑块的发展中可能比后者发挥更重要的作用。因此,EAT 可能作为一种旁分泌组织,作用于冠状动脉,促进局部炎症和动脉粥样硬化钙化。