PDF(Pubmed)
Abstract：
Obesity is a growing public health problem, with its prevalence rate having tripled in the last five decades. It has been shown that obesity is associated with alterations in cardiac energy metabolism, which in turn plays a significant role in heart failure development. During obesity, the heart becomes highly dependent on fatty acid oxidation as its primary source of energy (ATP), while the contribution from glucose oxidation significantly decreases. This metabolic inflexibility is associated with reduced cardiac efficiency and contractile dysfunction. Although it is well recognized that alterations in cardiac energy metabolism during obesity are associated with the risk of heart failure development, the molecular mechanisms controlling these metabolic changes are not fully understood. Recently, posttranslational protein modifications of metabolic enzymes have been shown to play a crucial role in cardiac energy metabolic changes seen in obesity. Understanding these novel mechanisms is important in developing new therapeutic options to treat or prevent cardiac metabolic alteration and dysfunction in obese individuals. This review discusses posttranslational acetylation changes during obesity and their roles in mediating cardiac energy metabolic perturbations during obesity as well as its therapeutic potentials.
摘要：
肥胖是一个日益严重的公共卫生问题，在过去的五十年里，它的患病率增加了两倍。研究表明，肥胖与心脏能量代谢的改变有关，这反过来在心力衰竭的发展中起着重要作用。在肥胖期间，心脏变得高度依赖脂肪酸氧化作为其主要能量来源（ATP），而葡萄糖氧化的贡献显著降低。这种代谢不灵活与心脏效率降低和收缩功能障碍有关。尽管人们公认肥胖期间心脏能量代谢的改变与心力衰竭发展的风险有关，控制这些代谢变化的分子机制尚未完全了解。最近,代谢酶的翻译后蛋白修饰已被证明在肥胖患者的心脏能量代谢变化中起着至关重要的作用.了解这些新机制对于开发新的治疗方案以治疗或预防肥胖个体的心脏代谢改变和功能障碍非常重要。这篇综述讨论了肥胖过程中翻译后乙酰化的变化及其在肥胖过程中介导心脏能量代谢扰动的作用及其治疗潜力。
