AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle
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AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle. / Li, Jingwen; Knudsen, Jonas Roland; Henriquez-Olguin, Carlos; Li, Zhencheng; Birk, Jesper Bratz; Persson, Kaspar Wredstrøm; Hellsten, Ylva; Offergeld, Anika; Jarassier, William; Grand, Fabien L; Schjerling, Peter; Wojtaszewski, Jørgen; Jensen, Thomas Elbenhardt.
I: Journal of Physiology, Bind 599, Nr. 12, 2021, s. 3081-3100.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle
AU - Li, Jingwen
AU - Knudsen, Jonas Roland
AU - Henriquez-Olguin, Carlos
AU - Li, Zhencheng
AU - Birk, Jesper Bratz
AU - Persson, Kaspar Wredstrøm
AU - Hellsten, Ylva
AU - Offergeld, Anika
AU - Jarassier, William
AU - Grand, Fabien L
AU - Schjerling, Peter
AU - Wojtaszewski, Jørgen
AU - Jensen, Thomas Elbenhardt
N1 - This article is protected by copyright. All rights reserved.
PY - 2021
Y1 - 2021
N2 - AXIN1 is a scaffold protein known to interact with >20 proteins in signal transduction pathways regulating cellular development and function. Recently, AXIN1 was proposed to assemble a protein complex essential to catabolic-anabolic transition by coordinating AMPK activation and inactivation of mTORC1 and to regulate glucose uptake-stimulation by both AMPK and insulin. To investigate whether AXIN1 is permissive for adult skeletal muscle function, a phenotypic in vivo and ex vivo characterization of tamoxifen-inducible skeletal muscle-specific AXIN1 knockout (AXIN1 imKO) mice was conducted. AXIN1 imKO did not influence AMPK/mTORC1 signaling or glucose uptake stimulation, neither at rest nor in response to different exercise/contraction protocols, pharmacological AMPK activation, insulin or amino acids stimulation. The only genotypic difference observed was in exercising gastrocnemius muscle, where AXIN1 imKO displayed elevated α2/β2/γ3 AMPK activity and AMP/ATP ratio compared to wild-type mice. Our work shows that AXIN1 imKO generally does not affect skeletal muscle AMPK/mTORC1 signaling and glucose metabolism, likely due to functional redundancy of its homolog AXIN2.
AB - AXIN1 is a scaffold protein known to interact with >20 proteins in signal transduction pathways regulating cellular development and function. Recently, AXIN1 was proposed to assemble a protein complex essential to catabolic-anabolic transition by coordinating AMPK activation and inactivation of mTORC1 and to regulate glucose uptake-stimulation by both AMPK and insulin. To investigate whether AXIN1 is permissive for adult skeletal muscle function, a phenotypic in vivo and ex vivo characterization of tamoxifen-inducible skeletal muscle-specific AXIN1 knockout (AXIN1 imKO) mice was conducted. AXIN1 imKO did not influence AMPK/mTORC1 signaling or glucose uptake stimulation, neither at rest nor in response to different exercise/contraction protocols, pharmacological AMPK activation, insulin or amino acids stimulation. The only genotypic difference observed was in exercising gastrocnemius muscle, where AXIN1 imKO displayed elevated α2/β2/γ3 AMPK activity and AMP/ATP ratio compared to wild-type mice. Our work shows that AXIN1 imKO generally does not affect skeletal muscle AMPK/mTORC1 signaling and glucose metabolism, likely due to functional redundancy of its homolog AXIN2.
U2 - 10.1113/JP281187
DO - 10.1113/JP281187
M3 - Journal article
C2 - 33913171
VL - 599
SP - 3081
EP - 3100
JO - The Journal of Physiology
JF - The Journal of Physiology
SN - 0022-3751
IS - 12
ER -
ID: 260992560