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Contractions but not AICAR increase FABPpm content in rat muscle sarcolemma

Jacob Jeppesen1, Peter Albers, Joost J Luiken

  • 1Molecular Physiology Group, Section of Human Physiology, Copenhagen Muscle Research Centre, Department of Exercise and Sports Sciences, The August Krogh Building, University of Copenhagen, Universitetsparken 13, 2100, Copenhagen, Denmark.

Molecular and Cellular Biochemistry
|January 15, 2009
PubMed
Abstract

Insights

Acute muscle contractions in rats increase plasma membrane protein content of fatty acid binding protein (FABPpm) and fatty acid translocase (FAT/CD36). AICAR stimulation only increases FAT/CD36, suggesting AMPK regulates FAT/CD36 but not FABPpm.

Area of Science:

  • Exercise Physiology
  • Molecular Biology
  • Skeletal Muscle Metabolism

Background:

  • Fatty acid transport proteins, including fatty acid binding protein (FABPpm) and fatty acid translocase (FAT/CD36), are crucial for energy substrate utilization in skeletal muscle.
  • Understanding the regulation of these proteins during muscle activity is essential for comprehending exercise-induced metabolic adaptations.

Purpose of the Study:

  • To investigate the impact of acute muscle contractions on FABPpm protein content in the plasma membrane of rat skeletal muscle.
  • To evaluate the effect of AICAR (AMPK activator) stimulation on FAT/CD36 and FABPpm protein content in the sarcolemma of rat skeletal muscle.

Main Methods:

  • Male Wistar rats underwent in situ electrically induced muscle contractions or AICAR stimulation.
  • The giant sarcolemma vesicle (GSV) technique was employed to isolate plasma membranes for analysis.
  • Western blotting was used to quantify protein content and phosphorylation status of key signaling molecules.

Main Results:

  • Electrical stimulation significantly increased FABPpm (61%) and FAT/CD36 (33%) protein content in GSVs.
  • AICAR stimulation increased FAT/CD36 (22%) but not FABPpm protein content in GSVs.
  • Muscle contractions and AICAR increased AMPK phosphorylation, while contractions also increased ERK1/2 phosphorylation.

Conclusions:

  • Skeletal muscle contractions enhance both FAT/CD36 and FABPpm protein levels in the plasma membrane.
  • AICAR stimulation selectively increases FAT/CD36, indicating AMPK's role in its regulation, but not FABPpm.
  • Both AMPK and ERK1/2 signaling pathways may contribute to the regulation of FABPpm and FAT/CD36 during muscle contractions.

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