Glucose restriction extends Caenorhabditis elegans life span by inducing mitochondrial respiration and increasing oxidative stress.

By T. Schulz, K. Zarse, A. Voigt, Nadine Urban, M. Birringer, Michael Ristow. Cell Metabolism, 2007

1,204 citations recorded by the source corpus.

Subfields: Aging, Endocrine and Autonomic Systems

View Paper: https://www.semanticscholar.org/paper/f3c098c66688d63c2d1b84a356dd766220e87643

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Aging

1. Toren Finkel
2. C. Kenyon
3. E. Verdin
4. Johan Auwerx
5. R. Houtkooper
6. L. Guarente
7. Brian Onken
8. Monica Driscoll

In Endocrine and Autonomic Systems

1. L. Guarente
2. R. Houtkooper
3. E. Verdin
4. Johan Auwerx
5. Brian Onken
6. Monica Driscoll
7. C. Kenyon
8. Toren Finkel

Citations in the corpus

• AMPK phosphorylation of raptor mediates a metabolic checkpoint. (2008, background): “elegans for lifespan extension by daf-2, heat shock, and glycolytic inhibitors (Apfeld et al., 2004; Schulz et al., 2007).”
• Mitochondrial ROS signaling in organismal homeostasis. (2015, background): “Ristow and colleagues broke new ground in this area by showing that reduced glucose availability leads to increased mitochondrial respiration and mtROS production that delays 562 Cell 163, October 22, 2015 ª2015 Elsevier Inc. worm aging (Schulz et al., 2007).”
• Acute exercise and oxidative stress: a 30 year history (2009, result): “To the contrary, and in accordance with the principle of hormesis, a low grade oxidative stress appears necessary for various physiological adaptations [35-37].”
• The NAD+/sirtuin pathway modulates longevity through activation of mitochondrial UPR and FOXO signaling (2013, background): “These days were selected based on the premise that they are in different phases of the mitohormesis response (Mouchiroud et al., 2011; Schulz et al., 2007; Zarse et al., 2012).”
• Calorie restriction reduces oxidative stress by SIRT3-mediated SOD2 activation. (2010, background): “Evidence is emerging to support the mitochondrial hormesis or ‘‘mitohormesis’’ concept, which hypothesizes that induction of mitochondrial metabolism and the increased formation of ROS trigger an active defense program, resulting in increased stress resistance and possibly extended life span (Schulz”
• Radical-free biology of oxidative stress. (2008, background): “The concept is supported by studies in Caenorhabditis elegans, which show that glucose restriction stimulated mitochondrial respiration and 2,7-dichlorodihydrofluoroscein diacetate oxidation and increased life span (155).”
• Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle (2010, background): “This link between AMPK and mitochondrial fitness might also explain why AMPK participates in the adaptations to other situations such as calorie restriction (Apfeld et al., 2004; Schulz et al., 2007).”
• Signal transduction by reactive oxygen species (2011, background): “In contrast, there are other models in lower organisms whereby the addition of low levels of ROS-producing compounds actually extends life (Schulz et al., 2007; Heidler et al., 2010; Lee et al., 2010; Yang and Hekimi, 2010), and where the genetic reduction of antioxidant defenses actually promotes a”
• Translational regulation of gene expression during conditions of cell stress. (2010, background): “For example, in Caenorhabditis elegans, life span is enhanced following glucose depletion by activating these stress pathways (Schulz et al., 2007), and under nutrient depletion in mammals there is an increase in mitochondrial biogenesis (Nisoli et al., 2005).”
• Antioxidants prevent health-promoting effects of physical exercise in humans (2009, background): “Evidence for this novel concept has been provided in model organisms such as nematodes (15) and rats (17), and the current study would extend the concept of mitohormesis to the amelioration of insulin resistance in humans, suggesting that potential harmful ROS may exert health promoting effects via ”
• Achieving the Balance between ROS and Antioxidants: When to Use the Synthetic Antioxidants (2013, background): “Paradoxically, the efficiency of defense and repair may be enhanced also after the exposure to ROS, since the expression of many DNA repair enzymes is upregulated during the oxidative stress [94–96].”