Division of Cardiology, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, Texas 77030, USA.
Am J Physiol Heart Circ Physiol. 2012 Apr 15;302(8):H1539-45. doi: 10.1152/ajpheart.00626.2011. Epub 2012 Feb 3.
Obesity is an independent risk factor for cardiovascular disease. Data from the Framingham Study have reported a higher incidence of heart failure in obese individuals compared with a normal cohort. The body initially copes with the abundance of fuel present in an obese milieu by storing it in adipose tissue. However, when the storage capacity is exceeded, the excess energy is taken up and stored ectopically as fat in vital organs such as the heart. Indeed, intramyocardial lipid overload is present in hearts of obese patients, as well as in hearts of animal models of obesity, and is associated with a distinct gene expression profile and cardiac dysfunction. By imposing a metabolic stress on the heart, obesity causes it to hypertrophy and ultimately to fail. Conventional measures to treat obesity include diet, exercise, and drugs. More recently, weight loss surgery (WLS) has achieved increasing prominence because of its ability to reduce the neurohumoral load, normalize metabolic dysregulation, and improve overall survival. The effects of WLS on systemic metabolic, neurohumoral, and hemodynamic parameters are well described and include an early normalization of serum glucose and insulin levels as well as reduction in blood pressure. WLS is also associated with reverse cardiac remodeling, regression of left ventricular hypertrophy, and improved left ventricular and right ventricular function. By targeting the source of the excess energy, we hypothesize that WLS improves contractile function by limiting exogenous substrate availability to the metabolically overloaded heart. These changes have also been found to be associated with increased levels of adiponectin and improved insulin sensitivity. Taken together, the sustained beneficial effects of WLS on left ventricular mass and function highlight the need to better understand the mechanism by which obesity regulates cardiovascular physiology.
肥胖是心血管疾病的一个独立危险因素。弗雷明汉研究的数据报告称，肥胖个体心力衰竭的发生率高于正常队列。身体最初通过将多余的燃料储存在脂肪组织中来应对肥胖环境中过多的燃料。然而，当储存能力超过时，多余的能量会被吸收并异位储存为心脏等重要器官的脂肪。事实上，肥胖患者的心脏以及肥胖动物模型的心脏中都存在心肌内脂质过载，并且与独特的基因表达谱和心脏功能障碍相关。肥胖通过向心脏施加代谢压力，导致其肥大并最终衰竭。治疗肥胖的传统方法包括饮食、运动和药物。最近，减肥手术（WLS）因其能够减轻神经激素负荷、使代谢失调正常化以及提高整体生存率而越来越受到关注。WLS 对全身代谢、神经激素和血液动力学参数的影响已有很好的描述，包括血清葡萄糖和胰岛素水平的早期正常化以及血压降低。WLS 还与心脏逆向重构、左心室肥厚消退以及左心室和右心室功能改善相关。通过针对多余能量的来源，我们假设 WLS 通过限制代谢超负荷心脏中外源底物的可用性来改善收缩功能。这些变化也与脂联素水平升高和胰岛素敏感性改善相关。综上所述，WLS 对左心室质量和功能的持续有益影响突出表明需要更好地理解肥胖调节心血管生理学的机制。
