摘要
采用文献资料法,对脂肪细胞内质网应激与运动介导的代谢适应机制进行研究,旨在为后续的临床病理研究和运动干预提供理论依据。结果显示:内质网是真核细胞内合成代谢的重要场所,当脂肪细胞受到应激后会触发ERS,未折叠与错误折叠的蛋白质在内质网中聚积,诱发UPR。UPR通过PERK、IRE1、ATF-6三种应激蛋白进行介导,通过抑制蛋白表达、上调伴侣蛋白等缓解ERS。UPR三条通路还可以通过JNK和NF-kB诱导脂肪因子与炎症因子的表达或紊乱,介导炎症反应。当应激持续进行时,通过CHOP和JNK通路触发细胞凋亡。持续性的炎症反应与细胞凋亡会加剧内质网应激,形成恶性循环,造成代谢性疾病的发生与发展。长期运动可以通过PGC-1α产生UCP1诱发体内ERS预适应,并增加适应性分子ATF6、eIF2α,减少凋亡相关基因XBP1、Bip的表达,增加机体抗损伤能力;且运动可通过降低JNK、NF-kB等信号降低IL-6、IL-15、TNF-α等炎性因子的表达,从而调节细胞内的炎症并改善脂肪因子的异常分泌,改善机体胰岛素抵抗,缓解甚至逆转代谢性疾病。
The mechanism of metabolic adaptation of adipocyte endoplasmic reticulum stress and exercise street was studied by using literature method in order to provide theoretical basis for follow-up clinical case study and exercise courage. Endoplasmic reticulum is an important site of eukaryotic cell for metabolism. When the adipose cells are stressed, Endoplasmic reticulum stess(ERS) is triggered, and the unfolded and misfolded proteins accumulate in the endoplasmic reticulum and induce Unfolded Protein Response(UPR). UPR is mediated by three proteins including PERK, IRE1, ATF-6, and the UPR can reduce ERS by inhibiting protein expression and up-regulation of chaperone protein. The three pathways of UPR can also induce inflammatory by the disorder of adipokines and inflammatory factors through JNK and NF-kB. And when the stress continues, apoptosis are triggered by the CHOP and JNK signal. Persistent inflammatory response and apoptosis will exacerbate the ERS and form a vicious cycle, resulting in the metabolic disorders. Long-term exercise can produce UCP1 that could induced ERS to preconditioning in vivo by PGC-1α;and exercise can increase the anti-injury ability of body by increase the expression of ATF6, eIF2α, and reduce the expression of apoptosis-related genes XBP1 and Bip;and exercise can reduce JNK, NF-KB and other inflammatory signals to reduce IL-6, IL-15, TNF-α and other factors, which regulate intracellular inflammation and improve the abnormal secretion of adipokines as well as body’s insulin resistance, remission or even reverse the metabolic diseases.
作者
叶群
朱小烽
马云
梁辰
高璨
张建红
YE Qun;ZHU Xiaofeng;MA Yun;LIANG Chen;GAO Can;ZHANG Jianhong(Sports Science School of Shanghai Physical Education Institute,Shanghai 200438,China;Normal School of Jiaxing College,Jiaxing 314200,Zhejiang,China;Sports Medical Research Institute of State General Administration of Sports,Beijing 100061,China)
出处
《辽宁体育科技》
2019年第1期50-58,共9页
Liaoning Sport Science and Technology
基金
"十二五"国家科技支撑计划项目(编号:2012BAK21B02-03)
关键词
脂肪细胞
内质网应激
代谢障碍
运动适应
adipocytes
endoplasmic reticulum stress
metabolic disorder
exercise
