PMID- 26527493
OWN - NLM
STAT- MEDLINE
DCOM- 20160830
LR  - 20151116
IS  - 1532-2777 (Electronic)
IS  - 0306-9877 (Linking)
VI  - 85
IP  - 6
DP  - 2015 Dec
TI  - Protective effects of exercise in metabolic disorders are mediated by inhibition 
      of mitochondrial-derived sterile inflammation.
PG  - 707-9
LID - S0306-9877(15)00408-9 [pii]
LID - 10.1016/j.mehy.2015.10.026 [doi]
AB  - While beneficial properties of physical activity and exercise on human health 
      have been extensively reported in literature, the exact mechanism(s) underpinning 
      impacts of exercise are not well understood. Focusing on metabolic disorders, as 
      the main causes of social and economic burden in current century, exercise 
      exhibited promising effects in prevention, alleviation and retardation of these 
      disorders including, type 2 diabetes (T2D), Alzheimer's disease (AD), major 
      depressive disorder (MDD) and obesity. Recent evidence has unmasked the role of 
      mitochondrial dysfunction and chronic inflammation in pathophysiology of these 
      disorders. Despite of the wealth of research on the etiology of metabolic 
      disorders, intimate connections between these diseases, complex pathophysiology 
      and their comorbidity still remains a challenging dilemma. In addition, although 
      physical activity has improving effects on human health, it is not clear that how 
      exercise is able to exert its modulatory effects on outcomes of metabolic 
      disorders. Among several mechanisms, we assumed the hypothesis that exercise 
      mitigates the production of mitochondrial-induced reactive oxygen species (ROS) 
      and danger associated molecular patterns (DAMPs) as the main triggering factors 
      for inflammasome formation. Since inflammasomes are of highly deleterious 
      molecules relevant to pathogenesis of metabolic disorders, we hypothesized that 
      beneficial effects of exercise may be associated with its ability to enhance the 
      mitochondrial biogenesis and glucose transportation through generation of brain 
      derived neurotrophic factor (BDNF). Also, we proposed that boosting impact of 
      exercise on autophagy process accelerates the elimination of damaged mitochondria 
      and thus, results in considerable decrease in production of ROS and DAMPs and 
      consequently sterile inflammation.
CI  - Copyright (c) 2015 Elsevier Ltd. All rights reserved.
FAU - Peeri, Maghsoud
AU  - Peeri M
AD  - Department of Exercise Physiology, Central Tehran Branch, Islamic Azad 
      University, Tehran, Iran. Electronic address: mpeeri@iauctb.ac.ir.
FAU - Amiri, Shayan
AU  - Amiri S
AD  - Department of Pharmacology, School of Medicine, Tehran University of Medical 
      Sciences, Tehran, Iran.
LA  - eng
PT  - Journal Article
DEP - 20151026
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Evidence-Based Medicine
MH  - Exercise Therapy/*methods
MH  - Humans
MH  - Immune Tolerance/immunology
MH  - Immunity, Innate
MH  - Inflammation/*immunology/prevention & control
MH  - Metabolic Diseases/diagnosis/*immunology/*prevention & control
MH  - Mitochondria/*immunology
MH  - Models, Immunological
MH  - Physical Exertion/immunology
MH  - Reactive Oxygen Species/immunology
MH  - Stress, Physiological/*immunology
MH  - Treatment Outcome
EDAT- 2015/11/04 06:00
MHDA- 2016/08/31 06:00
CRDT- 2015/11/04 06:00
PHST- 2015/09/07 00:00 [received]
PHST- 2015/10/06 00:00 [revised]
PHST- 2015/10/23 00:00 [accepted]
PHST- 2015/11/04 06:00 [entrez]
PHST- 2015/11/04 06:00 [pubmed]
PHST- 2016/08/31 06:00 [medline]
AID - S0306-9877(15)00408-9 [pii]
AID - 10.1016/j.mehy.2015.10.026 [doi]
PST - ppublish
SO  - Med Hypotheses. 2015 Dec;85(6):707-9. doi: 10.1016/j.mehy.2015.10.026. Epub 2015 
      Oct 26.