高强度间歇训练改善肥胖患者认知功能的线粒体机制研究进展

doi:10.12114/j.issn.1007-9572.2022.0239

中国全科医学 ›› 2022, Vol. 25 ›› Issue (29): 3702-3709.DOI: 10.12114/j.issn.1007-9572.2022.0239

所属专题：肥胖最新文章合集

高强度间歇训练改善肥胖患者认知功能的线粒体机制研究进展

蔡明¹^,², 王晓军³, 陈晓艳⁴, 胡静芸⁵^,^*()

1．201318　上海市，上海健康医学院康复学院
2．200240　上海市，上海交通大学Bio-X研究院
3．201615　上海市，上海赫尔森康复医院科教科
4．201615　上海市，上海赫尔森康复医院康复治疗管理科
5．201299　上海市浦东新区人民医院中心实验室　病原真菌医学检验中心

收稿日期:2022-01-14 修回日期:2022-04-20 出版日期:2022-10-15 发布日期:2022-05-06
通讯作者: 胡静芸
蔡明，王晓军，陈晓艳，等.高强度间歇训练改善肥胖患者认知功能的线粒体机制研究进展[J].中国全科医学，2022，25（29）：3702-3709. [www.chinagp.net]
作者贡献：蔡明负责文献和资料收集、论文撰写及论文图片制作；王晓军负责文章的质量控制及审校；陈晓艳负责文章的文献/资料整理；胡静芸负责研究命题的提出、设计及负责最终版本修订，对论文负责。所有作者确认论文终稿。
基金资助:
教育部人文社会科学研究青年基金项目（20YJCZH001）——"健康中国2030"战略下老年轻度认知障碍风险因素筛查模式构建及康复干预实证研究; 中国博士后基金面上项目（2021M702128）——间歇性低氧训练激活HIF-1α重塑AD早期海马能量代谢的机制研究; 横向科研项目（HXXM-21-03-005）——虚拟情景互动训练系统对卒中后轻度认知障碍的康复治疗效果验证; 上海市青年科技英才扬帆计划资助项目（22YF1441600）——乳酸在高强度间歇训练调控糖尿病脑病小鼠海马能量代谢中作用及机制探究

Latest Advances in the Mitochondrial Mechanism of High-intensity Interval Training Improving Obesity-induced Cognitive Impairment

Ming CAI¹^,², Xiaojun WANG³, Xiaoyan CHEN⁴, Jingyun HU⁵^,^*()

1. College of Rehabilitation Sciences, Shanghai University of Medicine & Health Sciences, Shanghai 201318, China
2. Bio-X Institutes, Shanghai Jiao Tong University, Shanghai 200240, China
3. Department of Science and Education, Shanghai Herson Rehabilitation Hospital, Shanghai 201615, China
4. Department of Rehabilitation Management, Shanghai Herson Rehabilitation Hospital, Shanghai 201615, China
5. Central Lab/Shanghai Key Laboratory of Pathogenic Fungi Medical Testing, Shanghai Pudong New Area People's Hospital, Shanghai 201299, China

Received:2022-01-14 Revised:2022-04-20 Published:2022-10-15 Online:2022-05-06
Contact: Jingyun HU
About author:
CAI M, WANG X J, CHEN X Y, et al. Latest advances in the mitochondrial mechanism of high-intensity interval training improving obesity-induced cognitive impairment[J]. Chinese General Practice, 2022, 25 (29) : 3702-3709.

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摘要/Abstract

摘要： 肥胖和相关的代谢变化已被证明是认知功能下降的重要危险因素并能损害认知功能，但潜在的神经生物学机制还未完全阐明。大量研究表明，肥胖个体脑内线粒体形态和功能出现异常改变。因此，脑线粒体功能障碍很可能是肥胖患者认知受损的潜在机制之一，而提高线粒体功能将是防治肥胖患者认知损伤的突破口。近年来高强度间歇训练（HIIT）被证明在肥胖健康管理、改善认知障碍方面卓有成效，可作为临床改善肥胖认知损伤的有效方法。HIIT对认知功能产生的有益效应常伴随脑内线粒体功能的提高。本文全面总结和讨论了线粒体功能和肥胖、HIIT之间的内在联系，以及HIIT改善肥胖个体认知损伤的线粒体机制，可为临床上应用HIIT治疗肥胖患者认知损伤提供理论基础。

关键词: 肥胖症, 认知功能障碍, 高强度间歇训练, 线粒体, 综述

Abstract:

Obesity and its related metabolic changes have proved to be important risk factors and causes for cognitive decline, but the potential neurobiological mechanisms remain incompletely clear. Numerous studies have shown that there are abnormal alterations in cerebral mitochondrial morphology and function in obese individuals. So cerebral mitochondrial dysfunction may be a probable mechanism for cognitive impairment in obesity, and improving which will be a breakthrough in the prevention and treatment of obesity-related cognitive impairment. High-intensity interval training (HIIT) has recently been proved to be effective in improving obesity-related health management and cognitive impairment, which may be used clinically as an efficient approach to improving obesity-related cognitive impairment. The cognitive benefits from HIIT are often manifested by improved cerebral mitochondrial function. We reviewed the latest advances in the internal relationship of cerebral mitochondrial function with obesity and HIIT, and the mitochondrial mechanism of HIIT improving obesity-related cognitive impairment, which may be evidence for clinical application of HIIT in the treatment of obesity-related cognitive impairment.

Key words: Obesity, Cognitive dysfunction, High-intensity interval training, Mitochondria, Review

蔡明,王晓军,陈晓艳,等. 高强度间歇训练改善肥胖患者认知功能的线粒体机制研究进展[J]. 中国全科医学, 2022, 25(29): 3702-3709. DOI: 10.12114/j.issn.1007-9572.2022.0239.
Ming CAI,Xiaojun WANG,Xiaoyan CHEN, et al. Latest Advances in the Mitochondrial Mechanism of High-intensity Interval Training Improving Obesity-induced Cognitive Impairment[J]. Chinese General Practice, 2022, 25(29): 3702-3709. DOI: 10.12114/j.issn.1007-9572.2022.0239.

图/表 2

图1 引起肥胖患者认知损伤的各因素与线粒体功能障碍间的联系注：High fat food=高脂饮食，Mitochondrial dysfunction=线粒体功能障碍，Mitochondrial swelling=线粒体肿胀，MMP=线粒体膜电位，ATP=三磷酸腺苷，ROS=活性氧，Oxygen consumption=耗氧量，Redox imbalance=氧化还原失衡，Brain=大脑，IR=胰岛素抵抗，Insulin signaling pathway=胰岛素信号通路，Insulin=胰岛素，Insulin receptor=胰岛素受体，IRS-1=胰岛素受体底物1，PI3K/AKT=磷脂酰肌醇激酶/蛋白激酶B，MAPK=丝裂原活化蛋白激酶，Neuroinflammation=神经炎症，NF-κB=核转录因子κB，NLRP3=NOD样受体蛋白3，IL-1β=白介素1β，TNF-α=肿瘤坏死因子α，Inflammatory signaling pathway=炎症信号通路，ERS=内质网应激，GRP78=葡萄糖调节蛋白78，PERK=蛋白激酶R样内质网激酶，IRE1α=肌醇酶1α，eIF2α=真核细胞起始因子2α，Oxidative stress=氧化应激，NRF2=核因子E2相关因子2，Keap1=Kelch样环氧氯丙烷相关蛋白1，Maf=肌肉腱膜纤维肉瘤，ARE=抗氧化反应元件，HO-1=血红素氧合酶1，NQO1=NAD(P)H：醌氧化还原酶1，SOD=超氧化物歧化酶，CAT=过氧化氢酶

Figure 1 The relationship of induction factors of obesity-related cognitive impairment with cerebral mitochondrial dysfunction

图2 HIIT促进认知功能的线粒体机制注：High-intensity interval training=高强度间歇训练，Mitochondrial biogenesis=线粒体生物发生，PGC-1α=过氧化物酶体增殖物激活受体γ共激活因子1α，TFAM=线粒体转录因子，mtDNA=线粒体DNA，Mitochondrial dysfunction=线粒体功能障碍，Cognitive function=认知功能

Figure 2 The possible mechanisms of high-intensity interval training on improving obesity-related cognitive impairment

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高强度间歇训练改善肥胖患者认知功能的线粒体机制研究进展

Latest Advances in the Mitochondrial Mechanism of High-intensity Interval Training Improving Obesity-induced Cognitive Impairment

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