Difference between revisions of "Schulz 2007 Cell Metab"
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{{Publication | {{Publication | ||
|title=Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M (2007) Glucose restriction extends ''Caenorhabditis elegans'' life span by inducing mitochondrial respiration and increasing oxidative stress. Cell Metab 6: 280- | |title=Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M (2007) Glucose restriction extends ''Caenorhabditis elegans'' life span by inducing mitochondrial respiration and increasing oxidative stress. Cell Metab 6:280-93. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/17908557 PMID: 17908557] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/17908557 PMID: 17908557] | ||
|authors=Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M | |authors=Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M | ||
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|organism=Caenorhabditis elegans | |organism=Caenorhabditis elegans | ||
|taxonomic group=Nematodes | |taxonomic group=Nematodes | ||
|preparations=Intact | |preparations=Intact organism | ||
|injuries=RONS | |injuries=Oxidative stress;RONS | ||
|diseases=Aging; senescence, Diabetes | |diseases=Aging;senescence, Diabetes | ||
|additional=Respiration, Diabetes | |additional=Respiration, Diabetes | ||
}} | }} |
Revision as of 16:41, 11 February 2015
Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M (2007) Glucose restriction extends Caenorhabditis elegans life span by inducing mitochondrial respiration and increasing oxidative stress. Cell Metab 6:280-93. |
Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M (2007) Cell Metab
Abstract: Increasing cellular glucose uptake is a fundamental concept in treatment of type 2 diabetes, whereas nutritive calorie restriction increases life expectancy. We show here that increased glucose availability decreases Caenorhabditis elegans life span, while impaired glucose metabolism extends life expectancy by inducing mitochondrial respiration. The histone deacetylase Sir2.1 is found here to be dispensable for this phenotype, whereas disruption of aak-2, a homolog of AMP-dependent kinase (AMPK), abolishes extension of life span due to impaired glycolysis. Reduced glucose availability promotes formation of reactive oxygen species (ROS), induces catalase activity, and increases oxidative stress resistance and survival rates, altogether providing direct evidence for a hitherto hypothetical concept named mitochondrial hormesis or "mitohormesis." Accordingly, treatment of nematodes with different antioxidants and vitamins prevents extension of life span. In summary, these data indicate that glucose restriction promotes mitochondrial metabolism, causing increased ROS formation and cumulating in hormetic extension of life span, questioning current treatments of type 2 diabetes as well as the widespread use of antioxidant supplements.
Labels:
Pathology: Aging;senescence, Diabetes
Stress:Oxidative stress;RONS
Organism: Caenorhabditis elegans
Preparation: Intact organism
Respiration, Diabetes