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Related Concept Videos

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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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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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Related Experiment Video

Updated: Oct 26, 2025

Assessment of the Metabolic Effects of Isocaloric 2:1 Intermittent Fasting in Mice
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Fasting increases 18:2-containing phosphatidylcholines to complement the decrease in 22:6-containing

Nanami Senoo1, Takumi Akahori1, Hiyori Ichida1

  • 1Laboratory of Nutritional Biochemistry, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Suruga-ku, Shizuoka, Japan.

Plos One
|July 26, 2021
PubMed
Summary

Fasting alters skeletal muscle phospholipids, decreasing 22:6-phosphatidylcholines (PCs) while increasing 18:2-PCs. This shift maintains total polyunsaturated fatty acid (PUFA)-containing PCs, indicating a compensatory adaptation in catabolic muscle states.

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Physiology

Background:

  • Skeletal muscle undergoes catabolic reactions during fasting to conserve energy.
  • Phospholipids, with diverse structures, influence cellular functions and are linked to muscle adaptation.
  • The impact of fasting on skeletal muscle phospholipid profiles is not well understood.

Purpose of the Study:

  • To investigate the effects of fasting on skeletal muscle phospholipid composition.
  • To identify specific phospholipid changes in response to nutrient deprivation.
  • To explore potential compensatory mechanisms in skeletal muscle phospholipids during fasting.

Main Methods:

  • Analysis of skeletal muscle phospholipids using liquid chromatography-mass spectrometry.
  • Comparison of phospholipid profiles in fasted versus non-fasted states.
  • Examination of phospholipid alterations in insulin-deficient mice and knockout models.

Main Results:

  • Fasting led to a decrease in 22:6-containing phosphatidylcholines (22:6-PCs) and an increase in 18:2-containing phosphatidylcholines (18:2-PCs).
  • The increase in 18:2-PCs compensated for the loss of 22:6-PCs, maintaining total polyunsaturated fatty acid (PUFA)-containing PCs.
  • Similar alterations were observed in insulin-deficient mice, suggesting a catabolic muscle characteristic.
  • Lysophosphatidic acid acyltransferase 3-knockout muscles showed an accumulation of 18:2-PCs, indicating a compensatory mechanism.

Conclusions:

  • Fasting induces specific changes in skeletal muscle phospholipid profiles, particularly in phosphatidylcholines.
  • Skeletal muscles exhibit compensatory mechanisms to maintain polyunsaturated fatty acid (PUFA) levels in phosphatidylcholines during fasting.
  • These findings provide insights into the molecular adaptations of skeletal muscle to nutrient deprivation.