AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle

Li, Jingwen, Knudsen, Jonas R., Henriquez-Olguin, Carlos, Li, Zhencheng, Birk, Jesper B., Persson, Kaspar W., Hellsten, Ylva, Offergeld, Anika ORCID: https://orcid.org/0000-0001-8916-2505, Jarassier, William, Le Grand, Fabien, Schjerling, Peter, Wojtaszewski, Jørgen F.P. and Jensen, Thomas E. 2021. AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle. Journal of Physiology 599 (12) , pp. 3081-3100. 10.1113/JP281187

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Abstract

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 signalling or glucose uptake stimulation at rest or 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 signalling and glucose metabolism, probably due to functional redundancy of its homologue AXIN2.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Publisher:	Wiley
ISSN:	0022-3751
Date of Acceptance:	20 April 2021
Last Modified:	06 May 2023 02:03
URI:	https://orca.cardiff.ac.uk/id/eprint/150636

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