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Related Concept Videos

Metabolic States of the Body: Fasting and Starvation01:24

Metabolic States of the Body: Fasting and Starvation

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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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Mitochondrial Membranes

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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...
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Mitochondria

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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Lipids also are sources of energy that power cellular processes. Like carbohydrates, lipids are composed of carbon, hydrogen, and oxygen, but these atoms are arranged differently. Most lipids are nonpolar and hydrophobic. Major types include fats and oils, waxes, phospholipids, and steroids.
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A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy
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Mitochondrial fission fueled by fasting.

Wei Wong1

  • 1Science Signaling, AAAS, Washington, DC 20005, USA.

Science Signaling
|August 8, 2023
PubMed
Summary

Fasting activates the mTORC2 pathway, promoting mitochondrial fission and enhancing cellular respiration. This process supports overall mitochondrial function during periods of nutrient deprivation.

Area of Science:

  • Cellular Biology
  • Metabolism
  • Mitochondrial Dynamics

Background:

  • Mitochondrial dynamics, including fission and fusion, are crucial for cellular health.
  • The mechanistic target of rapamycin (mTOR) pathway plays a key role in regulating cellular metabolism and growth.
  • The specific role of mTOR complex 2 (mTORC2) in regulating mitochondrial dynamics during fasting remains incompletely understood.

Purpose of the Study:

  • To investigate the role of mTORC2 in regulating mitochondrial fission during fasting.
  • To determine how mTORC2 activation by fasting impacts mitochondrial respiration.

Main Methods:

  • Utilized cell culture models and animal models of fasting.
  • Employed biochemical assays to measure mTORC2 activity.
  • Assessed mitochondrial morphology using microscopy.

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  • Quantified mitochondrial respiration through oxygen consumption rate measurements.

    • Main Results:

    • Fasting significantly activated mTORC2 signaling.
    • Activated mTORC2 promoted mitochondrial fission.
    • Increased mitochondrial fission correlated with enhanced mitochondrial respiration.
    • Inhibition of mTORC2 impaired fasting-induced mitochondrial fission and respiration.

    Conclusions:

    • Fasting-induced mTORC2 activation is a key regulator of mitochondrial fission.
    • mTORC2-mediated mitochondrial fission supports enhanced mitochondrial respiration during fasting.
    • These findings highlight a novel mechanism by which cells adapt metabolically to nutrient deprivation.