Dennis T. Villareal, MD, Baylor College of Medicine, Michael E DeBakey VA Medical Center, 2002 Holcombe Ave, Houston, TX 77030, USA, Email:
J Nutr Health Aging. 2023;27(5):312-313. doi: 10.1007/s12603-023-1922-0.
Through shared pathophysiologic mechanisms, obesity exacerbates the age-related decline in physical function, which leads to frailty and disability. Obesity and aging are characterized by chronic low-grade inflammation, which contributes to reduced muscle quality and protein control mechanisms as well as to diminished muscle anabolic response. Obesity causes oxidative stress and inflammation, which increases telomere shortening. Calorie excess increases ROS formation, which damages nucleus, endoplasmic reticulum, and mitochondria and promotes cellular senescence. Given the persistence of DNA damage associated with altered DNA repair proteins in obesity and aging, it is thought that inability to repair DNA may be the principal molecular event that underlies accelerated aging. Calorie restriction in combination with exercise slows biological aging by protecting against the molecular and cellular damages that occur in obesity and aging. Promising approaches such as Time Restricted Eating, Mediterranean Diet, and Senolytics need further investigation.
通过共同的病理生理机制，肥胖使与年龄相关的身体功能下降恶化，导致虚弱和残疾。肥胖和衰老的特点是慢性低度炎症，这导致肌肉质量和蛋白质控制机制下降，肌肉合成代谢反应减弱。肥胖导致氧化应激和炎症，从而导致端粒缩短。过量的热量会增加 ROS 的形成，从而损害细胞核、内质网和线粒体，并促进细胞衰老。鉴于与肥胖和衰老相关的 DNA 修复蛋白改变相关的 DNA 损伤的持续存在，人们认为无法修复 DNA 可能是导致加速衰老的主要分子事件。限制热量摄入与运动相结合，可以通过防止肥胖和衰老时发生的分子和细胞损伤来减缓生物衰老。限时进食、地中海饮食和 Senolytics 等有前途的方法需要进一步研究。
