Soltani Nakisa, Marandi Sayed Mohammad, Kazemi Mohammad, Esmaeil Nafiseh
Department of Exercise Physiology, Faculty of Sport Sciences, University of Isfahan, Isfahan, Iran.
Department of Genetics and Molecular Biology, Isfahan University of Medical Sciences, Isfahan, Iran.
Diabetes Metab Syndr Obes. 2020 Mar 19;13:785-810. doi: 10.2147/DMSO.S234992. eCollection 2020.
Reduced physical activity rate in people's lifestyle is a global concern associated with the prevalence of health disorders such as obesity and metabolic disturbance. Ample evidence has indicated a critical role of the immune system in the aggravation of obesity. The type, duration, and production of adipose tissue-released mediators may change subsequent inactive lifestyle-induced obesity, leading to the chronic systematic inflammation and monocyte/macrophage (MON/MФ) phenotype polarization. Preliminary adipose tissue expansion can be inhibited by changing the lifestyle. In this context, exercise training is widely recommended due to a definite improvement of energy balance and the potential impacts on the inflammatory signaling cascades. How exercise training affects the immune system has not yet been fully elucidated, because its anti-inflammatory, pro-inflammatory, or even immunosuppressive impacts have been indicated in the literature. A thorough understanding of the mechanisms triggered by exercise can suggest a new approach to combat meta-inflammation-induced metabolic diseases. In this review, we summarized the obesity-induced inflammatory pathways, the roles of MON/MФ polarization in adipose tissue and systemic inflammation, and the underlying inflammatory mechanisms triggered by exercise during obesity.
人们生活方式中体力活动率的降低是一个全球性问题,与肥胖和代谢紊乱等健康问题的流行相关。大量证据表明免疫系统在肥胖加重过程中起关键作用。脂肪组织释放介质的类型、持续时间和产生量可能会改变随后因不活动生活方式导致的肥胖,从而引发慢性全身炎症以及单核细胞/巨噬细胞(MON/MФ)表型极化。通过改变生活方式可以抑制脂肪组织的初步扩张。在此背景下,由于运动训练能明确改善能量平衡并对炎症信号级联反应产生潜在影响,因此被广泛推荐。运动训练如何影响免疫系统尚未完全阐明,因为文献中已表明其具有抗炎、促炎甚至免疫抑制作用。深入了解运动引发的机制可为对抗元炎症诱导的代谢性疾病提供新方法。在本综述中,我们总结了肥胖诱导的炎症途径、MON/MФ极化在脂肪组织和全身炎症中的作用,以及肥胖期间运动引发的潜在炎症机制。