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Related Concept Videos

Metabolic States of the Body: Fasting and Starvation01:24

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During the initial hours of fasting, the body uses up its glycogen stores as an energy source. Once these glycogen reserves are depleted, the body begins breaking down stored triglycerides and structural proteins. During this stage, glycerol becomes a key substrate for gluconeogenesis, while free fatty acids undergo beta-oxidation to provide energy for tissues, such as skeletal muscle. In the fasting state, the body spares protein breakdown as much as possible to conserve muscle and structural...
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Metabolic States of the Body: The Postabsorptive State01:18

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The postabsorptive state usually starts about four hours after a meal and lasts until the next meal is eaten. During this time, the digestive system stops absorbing nutrients, and the body uses stored energy reserves to maintain stable blood glucose levels.
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Fasting Drives Nrf2-Related Antioxidant Response in Skeletal Muscle.

Daniele Lettieri-Barbato1,2, Giuseppina Minopoli3, Rocco Caggiano3

  • 1Department of Biology, University of Rome Tor Vergata, via della Ricerca Scientifica, 00133 Rome, Italy.

International Journal of Molecular Sciences
|October 24, 2020
PubMed
Summary

Fasting activates protective antioxidant responses in skeletal muscle by inducing Nrf2-dependent genes. This metabolic adaptation reduces oxidative stress and lipid peroxidation, suggesting fasting as a beneficial approach for muscle health.

Keywords:
Nrf2lipid peroxidesmetabolismnutrient restrictionoxidative stress

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Area of Science:

  • Cellular Biology
  • Metabolism
  • Physiology

Background:

  • Fasting is a common metabolic state that triggers complex adaptive responses to maintain energy homeostasis.
  • Metabolic shifts during fasting can induce mild oxidative stress in skeletal muscle.
  • Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator of cellular stress responses.

Purpose of the Study:

  • To investigate the role of fasting as a protective mechanism against oxidative stress in skeletal muscle.
  • To elucidate the molecular pathways, particularly Nrf2-dependent mechanisms, involved in fasting-induced adaptations in skeletal muscle.

Main Methods:

  • Utilized in vivo and in vitro models to simulate fasting conditions.
  • Analyzed the expression of Nrf2-dependent genes involved in iron and glutathione metabolism.
  • Measured levels of antioxidant enzymes and markers of lipid peroxidation.

Main Results:

  • Fasting induced the expression of Nrf2-dependent genes, including Ho-1, Gcl, and Gsr, in skeletal muscle.
  • Increased levels of glutathione peroxidase 4 (Gpx4), a key antioxidant enzyme, were observed.
  • A significant reduction in malondialdehyde, a marker of lipid peroxidation, was detected.

Conclusions:

  • Fasting enhances adaptive antioxidant responses in skeletal muscle through Nrf2-dependent pathways.
  • These adaptations contribute to mitigating oxidative stress and lipid peroxidation in muscle tissue.
  • Fasting emerges as a potential strategy to bolster skeletal muscle's resilience against oxidative damage.