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• W2056525430 abstract "There is a body of evidence to refute James Watson's hypothesis suggesting that the reason for type 2 diabetes might be cellular oxidant production failure.1Watson JD Type 2 diabetes as a redox disease.Lancet. 2014; 383: 841-843Summary Full Text Full Text PDF PubMed Scopus (143) Google ScholarWerner syndrome is characterised by the premature onset of many processes associated with ageing. Patients with Werner syndrome show hallmarks of metabolic syndrome, including visceral obesity, hypertriglyceridaemia, insulin resistant type 2 diabetes, and associated cardiovascular diseases. Remarkably, the prominent findings of patients with Werner syndrome are increased reactive oxygen species (ROS) levels and genomic instability.2Massip L Garand C Paquet ER et al.Vitamin C restores healthy aging in a mouse model for Werner syndrome.FASEB J. 2010; 24: 158-172Crossref PubMed Scopus (90) Google Scholar Free radicals causing oxidative stress are inevitable byproducts of mitochondrial metabolism and have been proposed to exert repetitive damage to individual cells. However, exercise-induced repeated exposure to sublethal stress (ROS) has been proposed to enhance stress resistance and ultimately increased survival rates due to hormesis.3Ristow M Zarse K Oberbach A et al.Antioxidant prevents health-promoting effects of physical exercise in humans.Proc Natl Acad Sci USA. 2009; 106: 8665-8670Crossref PubMed Scopus (1149) Google Scholar The molecular mechanism behind the favourable effect of exercise could be linked to redox homoeostasis. The exercise-induced oxidative challenge-associated systemic adaptation mechanism is initiated by transcription factors, resulting in increased antioxidant enzymes, more effective repair and housekeeping by the DNA repair enzymes and proteasome complex.4Erol A Systemic DNA damage response and metabolic syndrome as a premalignant state.Curr Mol Med. 2010; 10: 321-334Crossref PubMed Scopus (53) Google Scholar Exercise-induced IGF-1 and PGC-1 production are other beneficial aspects of exercise, leading to increased production of mitochondria. They are also crucial in the maintenance of glucose, lipid, and energy homoeostasis.5Sandri M Lin J Handschin C et al.PGC1a protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription.Proc Natl Acad Sci USA. 2006; 103: 16260-16265Crossref PubMed Scopus (732) Google Scholar Finally, exercise-mediated stress activates the AMPK-p53 signalling pathway, which, in turn, decreases the systemic metabolic stress, inhibits mTORC1, and induces autophagy, which are considered beneficial for preventing age-associated pathologies (figure).4Erol A Systemic DNA damage response and metabolic syndrome as a premalignant state.Curr Mol Med. 2010; 10: 321-334Crossref PubMed Scopus (53) Google ScholarI declare no competing interests. There is a body of evidence to refute James Watson's hypothesis suggesting that the reason for type 2 diabetes might be cellular oxidant production failure.1Watson JD Type 2 diabetes as a redox disease.Lancet. 2014; 383: 841-843Summary Full Text Full Text PDF PubMed Scopus (143) Google Scholar Werner syndrome is characterised by the premature onset of many processes associated with ageing. Patients with Werner syndrome show hallmarks of metabolic syndrome, including visceral obesity, hypertriglyceridaemia, insulin resistant type 2 diabetes, and associated cardiovascular diseases. Remarkably, the prominent findings of patients with Werner syndrome are increased reactive oxygen species (ROS) levels and genomic instability.2Massip L Garand C Paquet ER et al.Vitamin C restores healthy aging in a mouse model for Werner syndrome.FASEB J. 2010; 24: 158-172Crossref PubMed Scopus (90) Google Scholar Free radicals causing oxidative stress are inevitable byproducts of mitochondrial metabolism and have been proposed to exert repetitive damage to individual cells. However, exercise-induced repeated exposure to sublethal stress (ROS) has been proposed to enhance stress resistance and ultimately increased survival rates due to hormesis.3Ristow M Zarse K Oberbach A et al.Antioxidant prevents health-promoting effects of physical exercise in humans.Proc Natl Acad Sci USA. 2009; 106: 8665-8670Crossref PubMed Scopus (1149) Google Scholar The molecular mechanism behind the favourable effect of exercise could be linked to redox homoeostasis. The exercise-induced oxidative challenge-associated systemic adaptation mechanism is initiated by transcription factors, resulting in increased antioxidant enzymes, more effective repair and housekeeping by the DNA repair enzymes and proteasome complex.4Erol A Systemic DNA damage response and metabolic syndrome as a premalignant state.Curr Mol Med. 2010; 10: 321-334Crossref PubMed Scopus (53) Google Scholar Exercise-induced IGF-1 and PGC-1 production are other beneficial aspects of exercise, leading to increased production of mitochondria. They are also crucial in the maintenance of glucose, lipid, and energy homoeostasis.5Sandri M Lin J Handschin C et al.PGC1a protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription.Proc Natl Acad Sci USA. 2006; 103: 16260-16265Crossref PubMed Scopus (732) Google Scholar Finally, exercise-mediated stress activates the AMPK-p53 signalling pathway, which, in turn, decreases the systemic metabolic stress, inhibits mTORC1, and induces autophagy, which are considered beneficial for preventing age-associated pathologies (figure).4Erol A Systemic DNA damage response and metabolic syndrome as a premalignant state.Curr Mol Med. 2010; 10: 321-334Crossref PubMed Scopus (53) Google Scholar I declare no competing interests. Type 2 diabetes as a redox diseasePhysical exercise has long been widely regarded as essential to human health.1 Yet, we do not know how exercise-stressed skeletal muscle cells that generate reactive oxygen species such as hydrogen peroxide (H2O2) delay—if not prevent—the occurrence and severity of diseases such as type 2 diabetes (as well as dementias, cardiovascular disease, and some cancers). Also unexplained is the recent finding that metformin—the most commonly used drug to treat type 2 diabetes2–4—and physical exercise seem to be beneficial for several of the same diseases, including cancer, Alzheimer's disease, and cardiovascular disease. Full-Text PDF" @default.
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• W2056525430 date "2014-09-01" @default.
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• W2056525430 title "Type 2 diabetes and cancer as redox diseases?" @default.
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