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AMPKα is critical for enhancing skeletal muscle fatty acid utilization during in vivo exercise in mice

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Fentz, J, Kjøbsted, R, Birk, JB, Jordy, AB, Jeppesen, J, Thorsen, K, Schjerling, P, Kiens, B, Jessen, N, Viollet, B & Wojtaszewski, JFP 2015, 'AMPKα is critical for enhancing skeletal muscle fatty acid utilization during in vivo exercise in mice' F A S E B Journal, bind 29, nr. 5, s. 1725-38. https://doi.org/10.1096/fj.14-266650

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Author

Fentz, Joachim ; Kjøbsted, Rasmus ; Birk, Jesper B ; Jordy, Andreas B ; Jeppesen, Jacob ; Thorsen, Kasper ; Schjerling, Peter ; Kiens, Bente ; Jessen, Niels ; Viollet, Benoit ; Wojtaszewski, Jørgen F P. / AMPKα is critical for enhancing skeletal muscle fatty acid utilization during in vivo exercise in mice. I: F A S E B Journal. 2015 ; Bind 29, Nr. 5. s. 1725-38.

Bibtex

@article{645b0f87dbd440709335a0e465576f52,
title = "AMPKα is critical for enhancing skeletal muscle fatty acid utilization during in vivo exercise in mice",
abstract = "The importance of AMPK in regulation of fatty acid (FA) oxidation in skeletal muscle with contraction/exercise is unresolved. Using a mouse model lacking both AMPKα1 and -α2 in skeletal muscle specifically (mdKO), we hypothesized that FA utilization would be impaired in skeletal muscle. AMPKα mdKO mice displayed normal respiratory exchange ratio (RER) when fed chow or a high-fat diet, or with prolonged fasting. However, in vivo treadmill exercise at the same relative intensity induced a higher RER in AMPKα mdKO mice compared to wild-type (WT = 0.81 ± 0.01 (sem); mdKO = 0.87 ± 0.02 (sem); P < 0.01), indicating a decreased utilization of FA. Further, ex vivo contraction-induced FA oxidation was impaired in AMPKα mdKO muscle, suggesting that the increased RER during exercise originated from decreased skeletal muscle FA oxidation. A decreased muscle protein expression of CD36 (cluster of differentiation 36) and FABPpm (plasma membrane fatty acid binding protein) (by ∼17-40{\%}), together with fully abolished TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) Ser(237) phosphorylation during contraction/exercise in AMPKα mdKO mice, may impair FA transport capacity and FA transport protein translocation to sarcolemma, respectively. AMPKα is thus required for normal FA metabolism during exercise and muscle contraction.",
keywords = "AMP-Activated Protein Kinases, Animals, Biomarkers, Blood Glucose, Fatty Acids, Female, Flow Cytometry, Gene Expression Profiling, Liver, Male, Mice, Mice, Knockout, Muscle Proteins, Muscle, Skeletal, Oligonucleotide Array Sequence Analysis, Phosphorylation, Physical Conditioning, Animal, Respiration",
author = "Joachim Fentz and Rasmus Kj{\o}bsted and Birk, {Jesper B} and Jordy, {Andreas B} and Jacob Jeppesen and Kasper Thorsen and Peter Schjerling and Bente Kiens and Niels Jessen and Benoit Viollet and Wojtaszewski, {J{\o}rgen F P}",
note = "{\circledC} FASEB.",
year = "2015",
month = "5",
doi = "10.1096/fj.14-266650",
language = "English",
volume = "29",
pages = "1725--38",
journal = "FASEB Journal",
issn = "0892-6638",
publisher = "Federation of American Societies for Experimental Biology",
number = "5",

}

RIS

TY - JOUR

T1 - AMPKα is critical for enhancing skeletal muscle fatty acid utilization during in vivo exercise in mice

AU - Fentz, Joachim

AU - Kjøbsted, Rasmus

AU - Birk, Jesper B

AU - Jordy, Andreas B

AU - Jeppesen, Jacob

AU - Thorsen, Kasper

AU - Schjerling, Peter

AU - Kiens, Bente

AU - Jessen, Niels

AU - Viollet, Benoit

AU - Wojtaszewski, Jørgen F P

N1 - © FASEB.

PY - 2015/5

Y1 - 2015/5

N2 - The importance of AMPK in regulation of fatty acid (FA) oxidation in skeletal muscle with contraction/exercise is unresolved. Using a mouse model lacking both AMPKα1 and -α2 in skeletal muscle specifically (mdKO), we hypothesized that FA utilization would be impaired in skeletal muscle. AMPKα mdKO mice displayed normal respiratory exchange ratio (RER) when fed chow or a high-fat diet, or with prolonged fasting. However, in vivo treadmill exercise at the same relative intensity induced a higher RER in AMPKα mdKO mice compared to wild-type (WT = 0.81 ± 0.01 (sem); mdKO = 0.87 ± 0.02 (sem); P < 0.01), indicating a decreased utilization of FA. Further, ex vivo contraction-induced FA oxidation was impaired in AMPKα mdKO muscle, suggesting that the increased RER during exercise originated from decreased skeletal muscle FA oxidation. A decreased muscle protein expression of CD36 (cluster of differentiation 36) and FABPpm (plasma membrane fatty acid binding protein) (by ∼17-40%), together with fully abolished TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) Ser(237) phosphorylation during contraction/exercise in AMPKα mdKO mice, may impair FA transport capacity and FA transport protein translocation to sarcolemma, respectively. AMPKα is thus required for normal FA metabolism during exercise and muscle contraction.

AB - The importance of AMPK in regulation of fatty acid (FA) oxidation in skeletal muscle with contraction/exercise is unresolved. Using a mouse model lacking both AMPKα1 and -α2 in skeletal muscle specifically (mdKO), we hypothesized that FA utilization would be impaired in skeletal muscle. AMPKα mdKO mice displayed normal respiratory exchange ratio (RER) when fed chow or a high-fat diet, or with prolonged fasting. However, in vivo treadmill exercise at the same relative intensity induced a higher RER in AMPKα mdKO mice compared to wild-type (WT = 0.81 ± 0.01 (sem); mdKO = 0.87 ± 0.02 (sem); P < 0.01), indicating a decreased utilization of FA. Further, ex vivo contraction-induced FA oxidation was impaired in AMPKα mdKO muscle, suggesting that the increased RER during exercise originated from decreased skeletal muscle FA oxidation. A decreased muscle protein expression of CD36 (cluster of differentiation 36) and FABPpm (plasma membrane fatty acid binding protein) (by ∼17-40%), together with fully abolished TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) Ser(237) phosphorylation during contraction/exercise in AMPKα mdKO mice, may impair FA transport capacity and FA transport protein translocation to sarcolemma, respectively. AMPKα is thus required for normal FA metabolism during exercise and muscle contraction.

KW - AMP-Activated Protein Kinases

KW - Animals

KW - Biomarkers

KW - Blood Glucose

KW - Fatty Acids

KW - Female

KW - Flow Cytometry

KW - Gene Expression Profiling

KW - Liver

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Muscle Proteins

KW - Muscle, Skeletal

KW - Oligonucleotide Array Sequence Analysis

KW - Phosphorylation

KW - Physical Conditioning, Animal

KW - Respiration

U2 - 10.1096/fj.14-266650

DO - 10.1096/fj.14-266650

M3 - Journal article

VL - 29

SP - 1725

EP - 1738

JO - FASEB Journal

JF - FASEB Journal

SN - 0892-6638

IS - 5

ER -

ID: 46032959