AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle
Key points Tamoxifen‐inducible skeletal muscle‐specific AXIN1 knockout (AXIN1 imKO) in mouse does not affect whole‐body energy substrate metabolism. AXIN1 imKO does not affect AICAR or insulin‐stimulated glucose uptake in adult skeletal muscle. AXIN1 imKO does not affect adult skeletal muscle AMPK o...
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| Veröffentlicht in: | The Journal of physiology 2021-06, Vol.599 (12), p.3081-3100 |
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| creator | Li, Jingwen Knudsen, Jonas R. Henriquez‐Olguin, Carlos Li, Zhencheng Birk, Jesper B. Persson, Kaspar W. Hellsten, Ylva Offergeld, Anika Jarassier, William Le Grand, Fabien Schjerling, Peter Wojtaszewski, Jørgen F.P. Jensen, Thomas E. |
| description | Key points
Tamoxifen‐inducible skeletal muscle‐specific AXIN1 knockout (AXIN1 imKO) in mouse does not affect whole‐body energy substrate metabolism.
AXIN1 imKO does not affect AICAR or insulin‐stimulated glucose uptake in adult skeletal muscle.
AXIN1 imKO does not affect adult skeletal muscle AMPK or mTORC1 signalling during AICAR/insulin/amino acid incubation, contraction and exercise.
During exercise, α2/β2/γ3AMPK and AMP/ATP ratio show greater increases in AXIN1 imKO than wild‐type in gastrocnemius muscle.
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.
Key points
Tamoxifen‐inducible skeletal muscle‐specific AXIN1 knockout (AXIN1 imKO) in mouse does not affect whole‐body energy substrate metabolism.
AXIN1 imKO does not affect AICAR or insulin‐stimulated glucose uptake in adult skeletal muscle.
AXIN1 imKO does not affect adult skeletal muscle AMPK or mTORC1 signalling during AICAR/insulin/amino acid incubation, contraction and exercise.
During exercise, α2/β2/γ3AMPK and AMP/ATP ratio show greater increases in AXIN1 imKO than wild‐type in gastrocnemius muscle. |
| doi_str_mv | 10.1113/JP281187 |
| format | Article |
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Tamoxifen‐inducible skeletal muscle‐specific AXIN1 knockout (AXIN1 imKO) in mouse does not affect whole‐body energy substrate metabolism.
AXIN1 imKO does not affect AICAR or insulin‐stimulated glucose uptake in adult skeletal muscle.
AXIN1 imKO does not affect adult skeletal muscle AMPK or mTORC1 signalling during AICAR/insulin/amino acid incubation, contraction and exercise.
During exercise, α2/β2/γ3AMPK and AMP/ATP ratio show greater increases in AXIN1 imKO than wild‐type in gastrocnemius muscle.
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.
Key points
Tamoxifen‐inducible skeletal muscle‐specific AXIN1 knockout (AXIN1 imKO) in mouse does not affect whole‐body energy substrate metabolism.
AXIN1 imKO does not affect AICAR or insulin‐stimulated glucose uptake in adult skeletal muscle.
AXIN1 imKO does not affect adult skeletal muscle AMPK or mTORC1 signalling during AICAR/insulin/amino acid incubation, contraction and exercise.
During exercise, α2/β2/γ3AMPK and AMP/ATP ratio show greater increases in AXIN1 imKO than wild‐type in gastrocnemius muscle.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/JP281187</identifier><identifier>PMID: 33913171</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Aminoimidazole Carboxamide ; AMP ; AMP-Activated Protein Kinases - metabolism ; AMPK ; Animals ; Axin Protein - genetics ; Contraction ; Energy Metabolism ; exercise ; Gastrocnemius muscle ; Glucose ; Glucose - metabolism ; Insulin ; Mechanistic Target of Rapamycin Complex 1 ; Metabolism ; Mice ; Mice, Knockout ; mTORC1 ; Muscle Contraction ; Muscle, Skeletal - physiology ; Musculoskeletal system ; Physical Conditioning, Animal ; Ribonucleotides ; Signal transduction ; Skeletal muscle</subject><ispartof>The Journal of physiology, 2021-06, Vol.599 (12), p.3081-3100</ispartof><rights>2021 The Authors. The Journal of Physiology © 2021 The Physiological Society</rights><rights>2021 The Authors. The Journal of Physiology © 2021 The Physiological Society.</rights><rights>Journal compilation © 2021 The Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3841-f2e28c22b3008901fef27e270661f60d8021fcc16ca88ac2a1a8907dba7ca1753</citedby><cites>FETCH-LOGICAL-c3841-f2e28c22b3008901fef27e270661f60d8021fcc16ca88ac2a1a8907dba7ca1753</cites><orcidid>0000-0002-7171-5172 ; 0000-0003-1475-5335 ; 0000-0002-5471-491X ; 0000-0002-9315-9365 ; 0000-0001-9557-3503 ; 0000-0001-6139-8268 ; 0000-0001-8185-3408 ; 0000-0002-2435-9558 ; 0000-0001-7138-3211</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1113%2FJP281187$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1113%2FJP281187$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33913171$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Jingwen</creatorcontrib><creatorcontrib>Knudsen, Jonas R.</creatorcontrib><creatorcontrib>Henriquez‐Olguin, Carlos</creatorcontrib><creatorcontrib>Li, Zhencheng</creatorcontrib><creatorcontrib>Birk, Jesper B.</creatorcontrib><creatorcontrib>Persson, Kaspar W.</creatorcontrib><creatorcontrib>Hellsten, Ylva</creatorcontrib><creatorcontrib>Offergeld, Anika</creatorcontrib><creatorcontrib>Jarassier, William</creatorcontrib><creatorcontrib>Le Grand, Fabien</creatorcontrib><creatorcontrib>Schjerling, Peter</creatorcontrib><creatorcontrib>Wojtaszewski, Jørgen F.P.</creatorcontrib><creatorcontrib>Jensen, Thomas E.</creatorcontrib><title>AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Key points
Tamoxifen‐inducible skeletal muscle‐specific AXIN1 knockout (AXIN1 imKO) in mouse does not affect whole‐body energy substrate metabolism.
AXIN1 imKO does not affect AICAR or insulin‐stimulated glucose uptake in adult skeletal muscle.
AXIN1 imKO does not affect adult skeletal muscle AMPK or mTORC1 signalling during AICAR/insulin/amino acid incubation, contraction and exercise.
During exercise, α2/β2/γ3AMPK and AMP/ATP ratio show greater increases in AXIN1 imKO than wild‐type in gastrocnemius muscle.
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.
Key points
Tamoxifen‐inducible skeletal muscle‐specific AXIN1 knockout (AXIN1 imKO) in mouse does not affect whole‐body energy substrate metabolism.
AXIN1 imKO does not affect AICAR or insulin‐stimulated glucose uptake in adult skeletal muscle.
AXIN1 imKO does not affect adult skeletal muscle AMPK or mTORC1 signalling during AICAR/insulin/amino acid incubation, contraction and exercise.
During exercise, α2/β2/γ3AMPK and AMP/ATP ratio show greater increases in AXIN1 imKO than wild‐type in gastrocnemius muscle.</description><subject>Aminoimidazole Carboxamide</subject><subject>AMP</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>AMPK</subject><subject>Animals</subject><subject>Axin Protein - genetics</subject><subject>Contraction</subject><subject>Energy Metabolism</subject><subject>exercise</subject><subject>Gastrocnemius muscle</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Insulin</subject><subject>Mechanistic Target of Rapamycin Complex 1</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>mTORC1</subject><subject>Muscle Contraction</subject><subject>Muscle, Skeletal - physiology</subject><subject>Musculoskeletal system</subject><subject>Physical Conditioning, Animal</subject><subject>Ribonucleotides</subject><subject>Signal transduction</subject><subject>Skeletal muscle</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kV1LIzEUhoMo264K_gIJeOPN6DlJO0kuS9FdXT_K0gXvhjRzpozNTHQyg_jvN0vtLix4deDl4eHlPYydIFwgory8XQiNqNUeG-MkN5lSRu6zMYAQmVRTHLGvMT4DoARjvrCRlAYlKhyzcvZ084B80wa3CUPPy0CRt6Hn1vfU8dn94sdls3z8OUfe0Xrwtq9Dy21b8rUfXIjEG-rtKvg6NrxueROGlMUN-RR73gzReTpiB5X1kY4_7iH7dX21nH_P7h6_3cxnd5mTeoJZJUhoJ8RKAmgDWFElFAkFeY5VDqUGgZVzmDurtXXCok2YKldWOYtqKg_Z-db70oXXgWJfNHV05L1tKfUqxBSNMlppndCz_9DnMHRtapeoCeSgDMA_oetCjB1VxUtXN7Z7LxCKP8sXu-UTevohHFYNlX_B3dQJuNgCb7Wn909FxfJ2kX6Yo_wNuMeJkA</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>Li, Jingwen</creator><creator>Knudsen, Jonas R.</creator><creator>Henriquez‐Olguin, Carlos</creator><creator>Li, Zhencheng</creator><creator>Birk, Jesper B.</creator><creator>Persson, Kaspar W.</creator><creator>Hellsten, Ylva</creator><creator>Offergeld, Anika</creator><creator>Jarassier, William</creator><creator>Le Grand, Fabien</creator><creator>Schjerling, Peter</creator><creator>Wojtaszewski, Jørgen F.P.</creator><creator>Jensen, Thomas E.</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7171-5172</orcidid><orcidid>https://orcid.org/0000-0003-1475-5335</orcidid><orcidid>https://orcid.org/0000-0002-5471-491X</orcidid><orcidid>https://orcid.org/0000-0002-9315-9365</orcidid><orcidid>https://orcid.org/0000-0001-9557-3503</orcidid><orcidid>https://orcid.org/0000-0001-6139-8268</orcidid><orcidid>https://orcid.org/0000-0001-8185-3408</orcidid><orcidid>https://orcid.org/0000-0002-2435-9558</orcidid><orcidid>https://orcid.org/0000-0001-7138-3211</orcidid></search><sort><creationdate>20210601</creationdate><title>AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle</title><author>Li, Jingwen ; Knudsen, Jonas R. ; Henriquez‐Olguin, Carlos ; Li, Zhencheng ; Birk, Jesper B. ; Persson, Kaspar W. ; Hellsten, Ylva ; Offergeld, Anika ; Jarassier, William ; Le Grand, Fabien ; Schjerling, Peter ; Wojtaszewski, Jørgen F.P. ; Jensen, Thomas E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3841-f2e28c22b3008901fef27e270661f60d8021fcc16ca88ac2a1a8907dba7ca1753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Aminoimidazole Carboxamide</topic><topic>AMP</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>AMPK</topic><topic>Animals</topic><topic>Axin Protein - genetics</topic><topic>Contraction</topic><topic>Energy Metabolism</topic><topic>exercise</topic><topic>Gastrocnemius muscle</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Insulin</topic><topic>Mechanistic Target of Rapamycin Complex 1</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>mTORC1</topic><topic>Muscle Contraction</topic><topic>Muscle, Skeletal - physiology</topic><topic>Musculoskeletal system</topic><topic>Physical Conditioning, Animal</topic><topic>Ribonucleotides</topic><topic>Signal transduction</topic><topic>Skeletal muscle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Jingwen</creatorcontrib><creatorcontrib>Knudsen, Jonas R.</creatorcontrib><creatorcontrib>Henriquez‐Olguin, Carlos</creatorcontrib><creatorcontrib>Li, Zhencheng</creatorcontrib><creatorcontrib>Birk, Jesper B.</creatorcontrib><creatorcontrib>Persson, Kaspar W.</creatorcontrib><creatorcontrib>Hellsten, Ylva</creatorcontrib><creatorcontrib>Offergeld, Anika</creatorcontrib><creatorcontrib>Jarassier, William</creatorcontrib><creatorcontrib>Le Grand, Fabien</creatorcontrib><creatorcontrib>Schjerling, Peter</creatorcontrib><creatorcontrib>Wojtaszewski, Jørgen F.P.</creatorcontrib><creatorcontrib>Jensen, Thomas E.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Jingwen</au><au>Knudsen, Jonas R.</au><au>Henriquez‐Olguin, Carlos</au><au>Li, Zhencheng</au><au>Birk, Jesper B.</au><au>Persson, Kaspar W.</au><au>Hellsten, Ylva</au><au>Offergeld, Anika</au><au>Jarassier, William</au><au>Le Grand, Fabien</au><au>Schjerling, Peter</au><au>Wojtaszewski, Jørgen F.P.</au><au>Jensen, Thomas E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>599</volume><issue>12</issue><spage>3081</spage><epage>3100</epage><pages>3081-3100</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>Key points
Tamoxifen‐inducible skeletal muscle‐specific AXIN1 knockout (AXIN1 imKO) in mouse does not affect whole‐body energy substrate metabolism.
AXIN1 imKO does not affect AICAR or insulin‐stimulated glucose uptake in adult skeletal muscle.
AXIN1 imKO does not affect adult skeletal muscle AMPK or mTORC1 signalling during AICAR/insulin/amino acid incubation, contraction and exercise.
During exercise, α2/β2/γ3AMPK and AMP/ATP ratio show greater increases in AXIN1 imKO than wild‐type in gastrocnemius muscle.
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.
Key points
Tamoxifen‐inducible skeletal muscle‐specific AXIN1 knockout (AXIN1 imKO) in mouse does not affect whole‐body energy substrate metabolism.
AXIN1 imKO does not affect AICAR or insulin‐stimulated glucose uptake in adult skeletal muscle.
AXIN1 imKO does not affect adult skeletal muscle AMPK or mTORC1 signalling during AICAR/insulin/amino acid incubation, contraction and exercise.
During exercise, α2/β2/γ3AMPK and AMP/ATP ratio show greater increases in AXIN1 imKO than wild‐type in gastrocnemius muscle.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>33913171</pmid><doi>10.1113/JP281187</doi><tpages>20</tpages><orcidid>https://orcid.org/0000-0002-7171-5172</orcidid><orcidid>https://orcid.org/0000-0003-1475-5335</orcidid><orcidid>https://orcid.org/0000-0002-5471-491X</orcidid><orcidid>https://orcid.org/0000-0002-9315-9365</orcidid><orcidid>https://orcid.org/0000-0001-9557-3503</orcidid><orcidid>https://orcid.org/0000-0001-6139-8268</orcidid><orcidid>https://orcid.org/0000-0001-8185-3408</orcidid><orcidid>https://orcid.org/0000-0002-2435-9558</orcidid><orcidid>https://orcid.org/0000-0001-7138-3211</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of physiology, 2021-06, Vol.599 (12), p.3081-3100 |
| issn | 0022-3751 1469-7793 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2519798788 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Wiley Online Library Free Content; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Aminoimidazole Carboxamide AMP AMP-Activated Protein Kinases - metabolism AMPK Animals Axin Protein - genetics Contraction Energy Metabolism exercise Gastrocnemius muscle Glucose Glucose - metabolism Insulin Mechanistic Target of Rapamycin Complex 1 Metabolism Mice Mice, Knockout mTORC1 Muscle Contraction Muscle, Skeletal - physiology Musculoskeletal system Physical Conditioning, Animal Ribonucleotides Signal transduction Skeletal muscle |
| title | AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle |
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