Activation of AMPK alpha2 is not required for mitochondrial FAT/CD36 accumulation during exercise

Journal article


Monaco, Cynthia, Whitfield, Jamie, Jain, Swati S., Spriet, Lawrence L., Bonen, Arend and Holloway, Graham P.. (2015) Activation of AMPK alpha2 is not required for mitochondrial FAT/CD36 accumulation during exercise. PLoS ONE. 10(5), pp. 1 - 15. https://doi.org/10.1371/journal.pone.0126122
AuthorsMonaco, Cynthia, Whitfield, Jamie, Jain, Swati S., Spriet, Lawrence L., Bonen, Arend and Holloway, Graham P.
Abstract

Exercise has been shown to induce the translocation of fatty acid translocase (FAT/CD36), a fatty acid transport protein, to both plasma and mitochondrial membranes. While previous studies have examined signals involved in the induction of FAT/CD36 translocation to sarcolemmal membranes, to date the signaling events responsible for FAT/CD36 accumulation on mitochondrial membranes have not been investigated. In the current study muscle contraction rapidly increased FAT/CD36 on plasma membranes (7.5 minutes), while in contrast, FAT/CD36 only increased on mitochondrial membranes after 22.5 minutes of muscle contraction, a response that was exercise-intensity dependent. Considering that previous research has shown that AMP activated protein kinase (AMPK) α2 is not required for FAT/CD36 translocation to the plasma membrane, we investigated whether AMPK α2 signaling is necessary for mitochondrial FAT/CD36 accumulation. Administration of 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) induced AMPK phosphorylation, and resulted in FAT/CD36 accumulation on SS mitochondria, suggesting AMPK signaling may mediate this response. However, SS mitochondrial FAT/CD36 increased following acute treadmill running in both wild-type (WT) and AMPKα 2 kinase dead (KD) mice. These data suggest that AMPK signaling is not required for SS mitochondrial FAT/CD36 accumulation. The current data also implicates alternative signaling pathways that are exercise-intensity dependent, as IMF mitochondrial FAT/CD36 content only occurred at a higher power output. Taken altogether the current data suggests that activation of AMPK signaling is sufficient but not required for exercise-induced accumulation in mitochondrial FAT/CD36.

Year2015
JournalPLoS ONE
Journal citation10 (5), pp. 1 - 15
PublisherPublic Library of Science
ISSN1932-6203
Digital Object Identifier (DOI)https://doi.org/10.1371/journal.pone.0126122
Scopus EID2-s2.0-84930659681
Open accessOpen access
Page range1 - 15
Research GroupMary MacKillop Institute for Health Research
Publisher's version
Additional information

[http://creativecommons.org/licenses/by/4.0/]
This work is licensed under a [http://creativecommons.org/licenses/by/4.0/] Creative Commons Attribution 4.0 International License.

Place of publicationUnited States of America
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