Exercise tolls the bell for key mediators of low-grade inflammation in dysmetabolic conditions. (December 2021)

• Record Type: Journal Article
• Authors: Della Guardia, Lucio; Codella, Roberto
• Is Part Of: Cytokine & growth factor reviews. Volume 62(2021)
• Page Start: 83
• Page End: 93
• Publication Date: 2021-12
• Subjects: AGEs advanced glycation end-products -- AKT Protein kinase B -- AMPK AMP-activated protein kinase -- BAT brown adipose tissue -- BDNF brain-derived neurotrophic factors -- FFAs fatty Free acids -- GLUT4 glucose transporter 4 -- HFD High fat diet -- IL-1β interleukin 1 Beta -- IL-10 interleukin 10 -- IL-6 Interleukin 6 -- IL-1ra Interleukin 1 receptor antagonist -- IRS insulin receptor substrates -- JAK Janus kinase. JNK 1–2, c-Jun n-terminal kinases 1 and 2 -- LPS lipopolysaccharide -- MCP-1 macrophage chemotactic protein 1 -- METRNL meteorin-like protein -- NF-κB nuclear factor kappa-light-chain-enhancer of activated B cells -- P38MAPK P38 mitogen-activated protein kinases -- PGC-1 Peroxisome proliferator-activated receptor gamma coactivator 1-alpha -- PPAR peroxisome proliferator-activated receptor -- RAGE Receptor of advanced glycation end-products -- MAPK Ras–mitogen-activated protein kinase -- SOCS3 suppressor of cytokine signaling 3 -- STAT signal transducer and activator of transcription -- T2D type 2 diabetes -- TLR toll-like receptor. TNFα, tumoral necrosis -- UCP uncoupling protein; Physical activity -- Cytokines -- Skeletal muscle -- Insulin resistance -- Adipose tissue -- Immune cells; Cytokines -- Periodicals; 571.84
• DOI: 10.1016/j.cytogfr.2021.09.003
• Languages: English
• ISSNs: 1359-6101

Abstract

Abstract: Metabolic conditions share a common low-grade inflammatory milieu, which represents a key-factor for their ignition and maintenance. Exercise is instrumental for warranting systemic cardio-metabolic balance, owing to its regulatory effect on inflammation. This review explores the effect of physical activity in the modulation of sub-inflammatory framework characterizing dysmetabolic conditions. Regular exercise suppresses plasma levels of TNFα, IL-1β, FFAs and MCP-1, in dysmetabolic subjects. In addition, a single session of training increases the anti-inflammatory IL-10, IL-1 receptor antagonist (IL-1ra), and muscle-derived IL-6, mitigating low-grade inflammation. Resting IL-6 levels are decreased in trained-dysmetabolic subjects, compared to sedentary. On the other hand, the acute release of muscle-IL-6, after exercise, seems to exert a regulatory effect on the metabolic and inflammatory balance. In fact, muscle-released IL-6 is presumably implicated in fat loss and boosts plasma levels of IL-10 and IL-1ra. The improvement of adipose tissue functionality, following regular exercise, is also critical for the mitigation of sub-inflammation. This effect is likely mediated by muscle-released IL-15 and IL-6 and partly relies on the brown-shifting of white adipocytes, induced by exercise. In obese-dysmetabolic subjects, moderate training is shown to restore gut-microbiota health, and this mitigates the translocation of bacterial-LPS into bloodstream. Finally, regular exercise can lower plasma advanced glycated endproducts. The articulated physiology of circulating mediators and the modulating effect of the pathophysiological background, render the comprehension of the exercise-regulatory effect on sub-inflammation a key issue, in dysmetabolism. Graphical Abstract: ga1 Highlights: In inactive subjects, adipose tissue-muscle crosstalk increases low-grade inflammation. Exercise-induced cytokines have a metabolic/inflammatory rebalancing effect. Exercise ameliorates low-grade inflammation by improving adipose tissue functionality. Regular exercise lowers plasma lipopolysaccharide concentration by improving gut health. Training decreases mediators of low-grade inflammation in healthy and dysmetabolic subjects.