The Role of Exercise-Induced Myokines in Muscle Homeostasis and the Defense against Chronic Diseases

被引:275
作者
Brandt, Claus [1 ]
Pedersen, Bente K. [1 ]
机构
[1] Univ Copenhagen, Fac Hlth Sci, Ctr Inflammat & Metab, Dept Infect Dis,Copenhagen Muscle Res Ctr,Rigshos, DK-2100 Copenhagen, Denmark
来源
JOURNAL OF BIOMEDICINE AND BIOTECHNOLOGY | 2010年
基金
英国医学研究理事会; 新加坡国家研究基金会;
关键词
NECROSIS-FACTOR-ALPHA; LIFE-STYLE INTERVENTION; NEUROTROPHIC FACTOR; SKELETAL-MUSCLE; PHYSICAL-ACTIVITY; TNF-ALPHA; INSULIN-RESISTANCE; COGNITIVE FUNCTION; DIABETES-MELLITUS; ENDOCRINE ORGAN;
D O I
10.1155/2010/520258
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Chronic inflammation is involved in the pathogenesis of insulin resistance, atherosclerosis, neurodegeneration, and tumour growth. Regular exercise offers protection against type 2 diabetes, cardiovascular diseases, colon cancer, breast cancer, and dementia. Evidence suggests that the protective effect of exercise may to some extent be ascribed to the antiinflammatory effect of regular exercise. Here we suggest that exercise may exert its anti-inflammatory effect via a reduction in visceral fat mass and/or by induction of an anti-inflammatory environment with each bout of exercise. According to our theory, such effects may in part be mediated via muscle-derived peptides, so-called "myokines". Contracting skeletal muscles release myokines with endocrine effects, mediating direct anti-inflammatory effects, and/or specific effects on visceral fat. Other myokines work locally within the muscle and exert their effects on signalling pathways involved in fat oxidation and glucose uptake. By mediating anti-inflammatory effects in the muscle itself, myokines may also counteract TNF-driven insulin resistance. In conclusion, exercise-induced myokines appear to be involved in mediating both systemic as well as local anti-inflammatory effects.
引用
收藏
页数:6
相关论文
共 53 条
[1]   The relationship between type 2 diabetes and cognitive dysfunction: longitudinal studies and their methodological limitations [J].
Allen, KV ;
Frier, BM ;
Strachan, MWJ .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2004, 490 (1-3) :169-175
[2]   Physical exercise at midlife and risk of dementia three decades later: A population-based study of Swedish twins [J].
Andel, Ross ;
Crowe, Michael ;
Pedersen, Nancy L. ;
Fratiglioni, Laura ;
Johansson, Boo ;
Gatz, Margaret .
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES, 2008, 63 (01) :62-66
[3]   Risk of dementia in diabetes mellitus: a systematic review [J].
Biessels, GJ ;
Staekenborg, S ;
Brunner, E ;
Brayne, C ;
Scheltens, P .
LANCET NEUROLOGY, 2006, 5 (01) :64-74
[4]   Exercise induces expression of leukaemia inhibitory factor in human skeletal muscle [J].
Broholm, Christa ;
Mortensen, Ole Hartvig ;
Nielsen, Soren ;
Akerstrom, Thorbjorn ;
Zankari, Alaa ;
Dahl, Benny ;
Pedersen, Bente Klarlund .
JOURNAL OF PHYSIOLOGY-LONDON, 2008, 586 (08) :2195-2201
[5]  
Bruunsgaard H, 1999, CLIN EXP IMMUNOL, V118, P235
[6]   Predicting death from tumour necrosis factor-alpha and interleukin-6 in 80-year-old people [J].
Bruunsgaard, H ;
Ladelund, S ;
Pedersen, AN ;
Schroll, M ;
Jorgensen, T ;
Pedersen, BK .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2003, 132 (01) :24-31
[7]   Age-related inflammatory cytokines and disease [J].
Brüünsgaard, H ;
Pedersen, BK .
IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA, 2003, 23 (01) :15-+
[8]  
BRUUNSGAARD H, 2000, AGEING IMMUNE FUNCTI
[9]   Brain-derived neurotrophic factor is reduced in Alzheimer's disease [J].
Connor, B ;
Young, D ;
Yan, Q ;
Faull, RLM ;
Synek, B ;
Dragunow, M .
MOLECULAR BRAIN RESEARCH, 1997, 49 (1-2) :71-81
[10]   The role of exercise and PGC1α in inflammation and chronic disease [J].
Handschin, Christoph ;
Spiegelman, Bruce M. .
NATURE, 2008, 454 (7203) :463-469