Food Security Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Department of Clinical Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran.
J Cachexia Sarcopenia Muscle. 2020 Dec;11(6):1447-1458. doi: 10.1002/jcsm.12611. Epub 2020 Aug 27.
Mitochondrial dysfunction can be a major cause of a wide range of age-related diseases. Maintaining the normal homeostasis of mitochondria population plays an important role in ensuring people's health, which is done through the mitophagy process. Among the various stimuli for the onset of mitophagy, caloric restriction (CR) is one of the strongest non-genetic triggers for initiating the mitophagy process. The primary objective of this paper is to review the literature assessing the effect of CR on mitophagy. Medline, Web of Science, Scopus, and Google Scholar databases was searched from inception to 1 August 2019. Reference lists from all selected articles were also examined for additional relevant studies. The evidence regarding the effect of fasting or CR on mitophagy is still limited. In addition, the methodological approaches of the studies are too heterogeneous in terms of types of food restriction, study duration, and targeted tissues. Most of the studies showed that fasting or CR induced mitophagy and mitophagy-related markers such as Binp3 and Parkin. However, some studies demonstrated that mitophagy occurred both in fasting and fed state with no significant differences or may be induced in fed state. Study on the muscle tissue of subjects after exercise showed that mitophagy was upregulated in the fed state. It has been demonstrated that mitophagy in the muscle was lowered in the absence of AMP-dependent kinase and fibroblast growth factor 21 genes, both in fasted and fed conditions. Current evidence overwhelmingly suggests that CR and fasting induce mitophagy and mitophagy-related markers. Based on the current evidence that we reviewed here, it could be concluded that fasting or CR has a promising role as a novel and practical approach in the prevention of age-related diseases without any side effects by inducing mitophagy in different organs of the body. More studies will be required in future to clarify the relationship between food deprivation and mitophagy. Further studies using a variety of different types of CR and fasting states are also warranted to determine the best approach for inducing mitophagy and improving health.
线粒体功能障碍可能是多种与年龄相关疾病的主要原因。维持线粒体群体的正常动态平衡对于确保人们的健康起着重要作用,这是通过自噬过程来实现的。在自噬发生的各种刺激中,热量限制(CR)是启动自噬过程的最强非遗传触发因素之一。本文的主要目的是综述评估 CR 对自噬影响的文献。从建库到 2019 年 8 月 1 日,我们在 Medline、Web of Science、Scopus 和 Google Scholar 数据库中进行了检索。还检查了所有选定文章的参考文献列表,以寻找其他相关研究。关于禁食或 CR 对自噬影响的证据仍然有限。此外,研究的方法学方法在食物限制类型、研究持续时间和靶向组织方面差异太大。大多数研究表明,禁食或 CR 诱导自噬和自噬相关标志物,如 Binp3 和 Parkin。然而,一些研究表明,自噬既发生在禁食状态也发生在进食状态,且没有显著差异,或者可能在进食状态下诱导。对运动后受试者肌肉组织的研究表明,在进食状态下自噬上调。已经证明,在禁食和进食条件下,AMP 依赖性激酶和成纤维细胞生长因子 21 基因缺失时,肌肉中的自噬会降低。目前的证据压倒性地表明,CR 和禁食诱导自噬和自噬相关标志物。基于我们在这里综述的现有证据,可以得出结论,禁食或 CR 通过在身体不同器官诱导自噬,作为一种预防与年龄相关疾病的新的实用方法,具有很大的潜力,而且没有任何副作用。未来需要进行更多的研究来阐明饥饿与自噬之间的关系。还需要进一步使用各种不同类型的 CR 和禁食状态进行研究,以确定诱导自噬和改善健康的最佳方法。