Insulin‐stimulated glucose uptake partly relies on p21‐activated kinase (PAK)2, but not PAK1, in mouse skeletal muscle
Key points Muscle‐specific genetic ablation of p21‐activated kinase (PAK)2, but not whole‐body PAK1 knockout, impairs glucose tolerance in mice. Insulin‐stimulated glucose uptake partly relies on PAK2 in glycolytic extensor digitorum longus muscle By contrast to previous reports, PAK1 is dispensable...
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| Veröffentlicht in: | The Journal of physiology 2020-12, Vol.598 (23), p.5351-5377 |
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| creator | Møller, Lisbeth L. V. Jaurji, Merna Kjøbsted, Rasmus Joseph, Giselle A. Madsen, Agnete B. Knudsen, Jonas R. Lundsgaard, Anne‐Marie Andersen, Nicoline R. Schjerling, Peter Jensen, Thomas E. Krauss, Robert S. Richter, Erik A. Sylow, Lykke |
| description | Key points
Muscle‐specific genetic ablation of p21‐activated kinase (PAK)2, but not whole‐body PAK1 knockout, impairs glucose tolerance in mice.
Insulin‐stimulated glucose uptake partly relies on PAK2 in glycolytic extensor digitorum longus muscle
By contrast to previous reports, PAK1 is dispensable for insulin‐stimulated glucose uptake in mouse muscle.
The group I p21‐activated kinase (PAK) isoforms PAK1 and PAK2 are activated in response to insulin in skeletal muscle and PAK1/2 signalling is impaired in insulin‐resistant mouse and human skeletal muscle. Interestingly, PAK1 has been suggested to be required for insulin‐stimulated glucose transporter 4 translocation in mouse skeletal muscle. Therefore, the present study aimed to examine the role of PAK1 in insulin‐stimulated muscle glucose uptake. The pharmacological inhibitor of group I PAKs, IPA‐3 partially reduced (–20%) insulin‐stimulated glucose uptake in isolated mouse soleus muscle (P |
| doi_str_mv | 10.1113/JP280294 |
| format | Article |
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Muscle‐specific genetic ablation of p21‐activated kinase (PAK)2, but not whole‐body PAK1 knockout, impairs glucose tolerance in mice.
Insulin‐stimulated glucose uptake partly relies on PAK2 in glycolytic extensor digitorum longus muscle
By contrast to previous reports, PAK1 is dispensable for insulin‐stimulated glucose uptake in mouse muscle.
The group I p21‐activated kinase (PAK) isoforms PAK1 and PAK2 are activated in response to insulin in skeletal muscle and PAK1/2 signalling is impaired in insulin‐resistant mouse and human skeletal muscle. Interestingly, PAK1 has been suggested to be required for insulin‐stimulated glucose transporter 4 translocation in mouse skeletal muscle. Therefore, the present study aimed to examine the role of PAK1 in insulin‐stimulated muscle glucose uptake. The pharmacological inhibitor of group I PAKs, IPA‐3 partially reduced (–20%) insulin‐stimulated glucose uptake in isolated mouse soleus muscle (P < 0.001). However, because there was no phenotype with genetic ablation of PAK1 alone, consequently, the relative requirement for PAK1 and PAK2 in whole‐body glucose homeostasis and insulin‐stimulated muscle glucose uptake was investigated. Whole‐body respiratory exchange ratio was largely unaffected in whole‐body PAK1 knockout (KO), muscle‐specific PAK2 KO and in mice with combined whole‐body PAK1 KO and muscle‐specific PAK2 KO. By contrast, glucose tolerance was mildly impaired in mice lacking PAK2 specifically in muscle, but not PAK1 KO mice. Moreover, while PAK1 KO muscles displayed normal insulin‐stimulated glucose uptake in vivo and in isolated muscle, insulin‐stimulated glucose uptake was slightly reduced in isolated glycolytic extensor digitorum longus muscle lacking PAK2 alone (–18%) or in combination with PAK1 KO (–12%) (P < 0.05). In conclusion, glucose tolerance and insulin‐stimulated glucose uptake partly rely on PAK2 in glycolytic mouse muscle, whereas PAK1 is dispensable for whole‐body glucose homeostasis and insulin‐stimulated muscle glucose uptake.
Key points
Muscle‐specific genetic ablation of p21‐activated kinase (PAK)2, but not whole‐body PAK1 knockout, impairs glucose tolerance in mice.
Insulin‐stimulated glucose uptake partly relies on PAK2 in glycolytic extensor digitorum longus muscle
By contrast to previous reports, PAK1 is dispensable for insulin‐stimulated glucose uptake in mouse muscle.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/JP280294</identifier><identifier>PMID: 32844438</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Animals ; Biological Transport ; Cyclin-dependent kinase inhibitor p21 ; Glucose ; Glucose - metabolism ; Glucose tolerance ; Glucose transporter ; glucose uptake ; GLUT4 translocation ; Glycolysis ; Homeostasis ; Insulin ; Insulin - metabolism ; Isoforms ; Kinases ; metabolism ; Mice ; Muscle, Skeletal - metabolism ; Musculoskeletal system ; p21-Activated Kinases - metabolism ; p21‐activated kinases ; Phenotypes ; Skeletal muscle ; Soleus muscle</subject><ispartof>The Journal of physiology, 2020-12, Vol.598 (23), p.5351-5377</ispartof><rights>2020 The Authors. The Journal of Physiology © 2020 The Physiological Society</rights><rights>2020 The Authors. The Journal of Physiology © 2020 The Physiological Society.</rights><rights>Journal compilation © 2020 The Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4782-e91e22bc42e1f5078bdadaf111a4f1c762c18c922102aca56c06d4ffc2b952ba3</citedby><cites>FETCH-LOGICAL-c4782-e91e22bc42e1f5078bdadaf111a4f1c762c18c922102aca56c06d4ffc2b952ba3</cites><orcidid>0000-0001-6139-8268 ; 0000-0002-7661-3335 ; 0000-0002-5471-491X ; 0000-0003-0905-5932 ; 0000-0002-6850-3056 ; 0000-0001-7138-3211 ; 0000-0003-1885-0102</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7771197/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7771197/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32844438$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Møller, Lisbeth L. V.</creatorcontrib><creatorcontrib>Jaurji, Merna</creatorcontrib><creatorcontrib>Kjøbsted, Rasmus</creatorcontrib><creatorcontrib>Joseph, Giselle A.</creatorcontrib><creatorcontrib>Madsen, Agnete B.</creatorcontrib><creatorcontrib>Knudsen, Jonas R.</creatorcontrib><creatorcontrib>Lundsgaard, Anne‐Marie</creatorcontrib><creatorcontrib>Andersen, Nicoline R.</creatorcontrib><creatorcontrib>Schjerling, Peter</creatorcontrib><creatorcontrib>Jensen, Thomas E.</creatorcontrib><creatorcontrib>Krauss, Robert S.</creatorcontrib><creatorcontrib>Richter, Erik A.</creatorcontrib><creatorcontrib>Sylow, Lykke</creatorcontrib><title>Insulin‐stimulated glucose uptake partly relies on p21‐activated kinase (PAK)2, but not PAK1, in mouse skeletal muscle</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Key points
Muscle‐specific genetic ablation of p21‐activated kinase (PAK)2, but not whole‐body PAK1 knockout, impairs glucose tolerance in mice.
Insulin‐stimulated glucose uptake partly relies on PAK2 in glycolytic extensor digitorum longus muscle
By contrast to previous reports, PAK1 is dispensable for insulin‐stimulated glucose uptake in mouse muscle.
The group I p21‐activated kinase (PAK) isoforms PAK1 and PAK2 are activated in response to insulin in skeletal muscle and PAK1/2 signalling is impaired in insulin‐resistant mouse and human skeletal muscle. Interestingly, PAK1 has been suggested to be required for insulin‐stimulated glucose transporter 4 translocation in mouse skeletal muscle. Therefore, the present study aimed to examine the role of PAK1 in insulin‐stimulated muscle glucose uptake. The pharmacological inhibitor of group I PAKs, IPA‐3 partially reduced (–20%) insulin‐stimulated glucose uptake in isolated mouse soleus muscle (P < 0.001). However, because there was no phenotype with genetic ablation of PAK1 alone, consequently, the relative requirement for PAK1 and PAK2 in whole‐body glucose homeostasis and insulin‐stimulated muscle glucose uptake was investigated. Whole‐body respiratory exchange ratio was largely unaffected in whole‐body PAK1 knockout (KO), muscle‐specific PAK2 KO and in mice with combined whole‐body PAK1 KO and muscle‐specific PAK2 KO. By contrast, glucose tolerance was mildly impaired in mice lacking PAK2 specifically in muscle, but not PAK1 KO mice. Moreover, while PAK1 KO muscles displayed normal insulin‐stimulated glucose uptake in vivo and in isolated muscle, insulin‐stimulated glucose uptake was slightly reduced in isolated glycolytic extensor digitorum longus muscle lacking PAK2 alone (–18%) or in combination with PAK1 KO (–12%) (P < 0.05). In conclusion, glucose tolerance and insulin‐stimulated glucose uptake partly rely on PAK2 in glycolytic mouse muscle, whereas PAK1 is dispensable for whole‐body glucose homeostasis and insulin‐stimulated muscle glucose uptake.
Key points
Muscle‐specific genetic ablation of p21‐activated kinase (PAK)2, but not whole‐body PAK1 knockout, impairs glucose tolerance in mice.
Insulin‐stimulated glucose uptake partly relies on PAK2 in glycolytic extensor digitorum longus muscle
By contrast to previous reports, PAK1 is dispensable for insulin‐stimulated glucose uptake in mouse muscle.</description><subject>Animals</subject><subject>Biological Transport</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glucose tolerance</subject><subject>Glucose transporter</subject><subject>glucose uptake</subject><subject>GLUT4 translocation</subject><subject>Glycolysis</subject><subject>Homeostasis</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Isoforms</subject><subject>Kinases</subject><subject>metabolism</subject><subject>Mice</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Musculoskeletal system</subject><subject>p21-Activated Kinases - metabolism</subject><subject>p21‐activated kinases</subject><subject>Phenotypes</subject><subject>Skeletal muscle</subject><subject>Soleus muscle</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kdtqFTEUhoModlsFn0AC3lTo1GQlM5m5EUrx0FpwX9TrkMlkarozmWkOle2Vj-Az-iRGe_AAXoWwvvWxfn6EnlJyQCllL0_W0BLo-D20orzpKiE6dh-tCAGomKjpDnoU4wUhlJGue4h2GLScc9au0JdjH7Oz_vvXbzHZKTuVzIDPXdZzNDgvSW0MXlRIbouDcdZEPHu8AC0LSid79YvfWK8Kvrc-fP8C9nGfE_ZzwuVL97H1eJpzGceNcSYph6cctTOP0YNRuWie3Ly76OOb12dH76rTD2-Pjw5PK81FC5XpqAHoNQdDx5qIth_UoMaSW_GRatGApq3uACgBpVXdaNIMfBw19F0NvWK76NW1d8n9ZAZtfArKySXYSYWtnJWVf0-8_STP5ysphKC0E0WwdyMI82U2McnJRm2cU96UYBI4E5ww0kBBn_-DXsw5-BKvUE1dN1AT8luowxxjMOPdMZTIn4XK20IL-uzP4-_A2wYLcHANfLbObP8rkmcna8pZDewHMf-rHA</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Møller, Lisbeth L. 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V. ; Jaurji, Merna ; Kjøbsted, Rasmus ; Joseph, Giselle A. ; Madsen, Agnete B. ; Knudsen, Jonas R. ; Lundsgaard, Anne‐Marie ; Andersen, Nicoline R. ; Schjerling, Peter ; Jensen, Thomas E. ; Krauss, Robert S. ; Richter, Erik A. ; Sylow, Lykke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4782-e91e22bc42e1f5078bdadaf111a4f1c762c18c922102aca56c06d4ffc2b952ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Biological Transport</topic><topic>Cyclin-dependent kinase inhibitor p21</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Glucose tolerance</topic><topic>Glucose transporter</topic><topic>glucose uptake</topic><topic>GLUT4 translocation</topic><topic>Glycolysis</topic><topic>Homeostasis</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Isoforms</topic><topic>Kinases</topic><topic>metabolism</topic><topic>Mice</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Musculoskeletal system</topic><topic>p21-Activated Kinases - metabolism</topic><topic>p21‐activated kinases</topic><topic>Phenotypes</topic><topic>Skeletal muscle</topic><topic>Soleus muscle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Møller, Lisbeth L. V.</creatorcontrib><creatorcontrib>Jaurji, Merna</creatorcontrib><creatorcontrib>Kjøbsted, Rasmus</creatorcontrib><creatorcontrib>Joseph, Giselle A.</creatorcontrib><creatorcontrib>Madsen, Agnete B.</creatorcontrib><creatorcontrib>Knudsen, Jonas R.</creatorcontrib><creatorcontrib>Lundsgaard, Anne‐Marie</creatorcontrib><creatorcontrib>Andersen, Nicoline R.</creatorcontrib><creatorcontrib>Schjerling, Peter</creatorcontrib><creatorcontrib>Jensen, Thomas E.</creatorcontrib><creatorcontrib>Krauss, Robert S.</creatorcontrib><creatorcontrib>Richter, Erik A.</creatorcontrib><creatorcontrib>Sylow, Lykke</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Møller, Lisbeth L. V.</au><au>Jaurji, Merna</au><au>Kjøbsted, Rasmus</au><au>Joseph, Giselle A.</au><au>Madsen, Agnete B.</au><au>Knudsen, Jonas R.</au><au>Lundsgaard, Anne‐Marie</au><au>Andersen, Nicoline R.</au><au>Schjerling, Peter</au><au>Jensen, Thomas E.</au><au>Krauss, Robert S.</au><au>Richter, Erik A.</au><au>Sylow, Lykke</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin‐stimulated glucose uptake partly relies on p21‐activated kinase (PAK)2, but not PAK1, in mouse skeletal muscle</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2020-12-01</date><risdate>2020</risdate><volume>598</volume><issue>23</issue><spage>5351</spage><epage>5377</epage><pages>5351-5377</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>Key points
Muscle‐specific genetic ablation of p21‐activated kinase (PAK)2, but not whole‐body PAK1 knockout, impairs glucose tolerance in mice.
Insulin‐stimulated glucose uptake partly relies on PAK2 in glycolytic extensor digitorum longus muscle
By contrast to previous reports, PAK1 is dispensable for insulin‐stimulated glucose uptake in mouse muscle.
The group I p21‐activated kinase (PAK) isoforms PAK1 and PAK2 are activated in response to insulin in skeletal muscle and PAK1/2 signalling is impaired in insulin‐resistant mouse and human skeletal muscle. Interestingly, PAK1 has been suggested to be required for insulin‐stimulated glucose transporter 4 translocation in mouse skeletal muscle. Therefore, the present study aimed to examine the role of PAK1 in insulin‐stimulated muscle glucose uptake. The pharmacological inhibitor of group I PAKs, IPA‐3 partially reduced (–20%) insulin‐stimulated glucose uptake in isolated mouse soleus muscle (P < 0.001). However, because there was no phenotype with genetic ablation of PAK1 alone, consequently, the relative requirement for PAK1 and PAK2 in whole‐body glucose homeostasis and insulin‐stimulated muscle glucose uptake was investigated. Whole‐body respiratory exchange ratio was largely unaffected in whole‐body PAK1 knockout (KO), muscle‐specific PAK2 KO and in mice with combined whole‐body PAK1 KO and muscle‐specific PAK2 KO. By contrast, glucose tolerance was mildly impaired in mice lacking PAK2 specifically in muscle, but not PAK1 KO mice. Moreover, while PAK1 KO muscles displayed normal insulin‐stimulated glucose uptake in vivo and in isolated muscle, insulin‐stimulated glucose uptake was slightly reduced in isolated glycolytic extensor digitorum longus muscle lacking PAK2 alone (–18%) or in combination with PAK1 KO (–12%) (P < 0.05). In conclusion, glucose tolerance and insulin‐stimulated glucose uptake partly rely on PAK2 in glycolytic mouse muscle, whereas PAK1 is dispensable for whole‐body glucose homeostasis and insulin‐stimulated muscle glucose uptake.
Key points
Muscle‐specific genetic ablation of p21‐activated kinase (PAK)2, but not whole‐body PAK1 knockout, impairs glucose tolerance in mice.
Insulin‐stimulated glucose uptake partly relies on PAK2 in glycolytic extensor digitorum longus muscle
By contrast to previous reports, PAK1 is dispensable for insulin‐stimulated glucose uptake in mouse muscle.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>32844438</pmid><doi>10.1113/JP280294</doi><tpages>27</tpages><orcidid>https://orcid.org/0000-0001-6139-8268</orcidid><orcidid>https://orcid.org/0000-0002-7661-3335</orcidid><orcidid>https://orcid.org/0000-0002-5471-491X</orcidid><orcidid>https://orcid.org/0000-0003-0905-5932</orcidid><orcidid>https://orcid.org/0000-0002-6850-3056</orcidid><orcidid>https://orcid.org/0000-0001-7138-3211</orcidid><orcidid>https://orcid.org/0000-0003-1885-0102</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of physiology, 2020-12, Vol.598 (23), p.5351-5377 |
| issn | 0022-3751 1469-7793 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7771197 |
| source | MEDLINE; Wiley Free Archive; Wiley Online Library Journals; PubMed Central; EZB Electronic Journals Library |
| subjects | Animals Biological Transport Cyclin-dependent kinase inhibitor p21 Glucose Glucose - metabolism Glucose tolerance Glucose transporter glucose uptake GLUT4 translocation Glycolysis Homeostasis Insulin Insulin - metabolism Isoforms Kinases metabolism Mice Muscle, Skeletal - metabolism Musculoskeletal system p21-Activated Kinases - metabolism p21‐activated kinases Phenotypes Skeletal muscle Soleus muscle |
| title | Insulin‐stimulated glucose uptake partly relies on p21‐activated kinase (PAK)2, but not PAK1, in mouse skeletal muscle |
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