肥胖是一个全球性的健康问题,因为它与许多退行性疾病相关,并且它可能导致早期衰老。衰老的各种标志,包括端粒损耗,表观遗传改变,改变蛋白质稳态,线粒体功能障碍,细胞衰老,干细胞疾病,和细胞间通讯,受肥胖的影响。因此,迫切需要安全有效的方法来预防肥胖和减轻过早衰老的发生。近年来,间歇性禁食(IF),在禁食和进食之间交替的饮食策略,已成为一种有前途的饮食策略,具有抵消与肥胖相关的衰老过程的潜力。本文探讨了IF影响肥胖相关早期衰老的分子和细胞机制。IF调节各种生理过程和器官系统,包括肝脏,大脑,肌肉,肠子,血,脂肪组织,内分泌系统,和心血管系统。此外,IF调节关键信号通路,如AMP激活的蛋白激酶(AMPK),sirtuins,磷脂酰肌醇3-激酶(PI3K)/Akt,哺乳动物雷帕霉素靶蛋白(mTOR),和叉头箱O(FOXO)。通过瞄准这些途径,IF具有减弱与肥胖相关的早期衰老相关的衰老表型的潜力。总的来说,IF为促进更健康的生活方式和减轻受肥胖影响的个体的过早衰老过程提供了有希望的途径。
Obesity is a global health concern owing to its association with numerous degenerative diseases and the fact that it may lead to early aging. Various markers of aging, including telomere attrition, epigenetic alterations, altered protein homeostasis, mitochondrial dysfunction, cellular senescence, stem cell disorders, and intercellular communication, are influenced by obesity. Consequently, there is a critical need for safe and effective approaches to prevent obesity and mitigate the onset of premature aging. In recent years, intermittent fasting (IF), a dietary strategy that alternates between periods of fasting and feeding, has emerged as a promising dietary strategy that holds potential in counteracting the aging process associated with obesity. This article explores the molecular and cellular mechanisms through which IF affects obesity-related early aging. IF regulates various physiological processes and organ systems, including the liver, brain, muscles, intestines, blood, adipose tissues, endocrine system, and cardiovascular system. Moreover, IF modulates key signaling pathways such as AMP-activated protein kinase (AMPK), sirtuins, phosphatidylinositol 3-kinase (PI3K)/Akt, mammalian target of rapamycin (mTOR), and fork head box O (FOXO). By targeting these pathways, IF has the potential to attenuate aging phenotypes associated with obesity-related early aging. Overall, IF offers promising avenues for promoting healthier lifestyles and mitigating the premature aging process in individuals affected by obesity.