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Article: Adiponectin is expressed by skeletal muscle fibers and influences muscle phenotype and function

TitleAdiponectin is expressed by skeletal muscle fibers and influences muscle phenotype and function
Authors
KeywordsIntramyocellular lipid
Muscle lipids
Muscle stimulation
Obesity
Type 2 diabetes
Issue Date2008
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
Citation
American Journal Of Physiology - Cell Physiology, 2008, v. 295 n. 1, p. C203-C212 How to Cite?
AbstractAdiponectin (Ad) is linked to various disease states and mediates antidiabetic and anti-inflammatory effects. While it was originally thought that Ad expression was limited to adipocytes, we demonstrate here that Ad is expressed in mouse skeletal muscles and within differentiated L6 myotubes, as assessed by RT-PCR, Western blot, and immunohistochemical analyses. Serial muscle sections stained for fiber type, lipid content, and Ad revealed that muscle fibers with elevated intramyocellular Ad expression were consistently type IIA and IID fibers with detectably higher intramyocellular lipid (IMCL) content. To determine the effect of Ad on muscle phenotype and function, we used an Ad-null [knockout (KO)] mouse model. Body mass increased significantly in 24-wk-old KO mice [+5.5 ± 3% relative to wild-type mice (WT)], with no change in muscle mass observed. IMCL content was significantly increased (+75.1 ± 25%), whereas epididymal fat mass, although elevated, was not different in the KO mice compared with WT (+35.1 ± 23%; P = 0.16). Fiber-type composition was unaltered, although type IIB fiber area was increased in KO mice (+25.5 ± 6%). In situ muscle stimulation revealed lower peak tetanic forces in KO mice relative to WT (-47.5 ± 6%), with no change in low-frequency fatigue rates. These data demonstrate that the absence of Ad expression causes contractile dysfunction and phenotypical changes in skeletal muscle. Furthermore, we demonstrate that Ad is expressed in skeletal muscle and that its intramyocellular localization is associated with elevated IMCL, particularly in type IIA/D fibers. Copyright © 2008 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/76568
ISSN
2021 Impact Factor: 5.282
2020 SCImago Journal Rankings: 1.432
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKrause, MPen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorVu, Ven_HK
dc.contributor.authorChan, Len_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorRiddell, MCen_HK
dc.contributor.authorSweeney, Gen_HK
dc.contributor.authorHawke, TJen_HK
dc.date.accessioned2010-09-06T07:22:37Z-
dc.date.available2010-09-06T07:22:37Z-
dc.date.issued2008en_HK
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 2008, v. 295 n. 1, p. C203-C212en_HK
dc.identifier.issn0363-6143en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76568-
dc.description.abstractAdiponectin (Ad) is linked to various disease states and mediates antidiabetic and anti-inflammatory effects. While it was originally thought that Ad expression was limited to adipocytes, we demonstrate here that Ad is expressed in mouse skeletal muscles and within differentiated L6 myotubes, as assessed by RT-PCR, Western blot, and immunohistochemical analyses. Serial muscle sections stained for fiber type, lipid content, and Ad revealed that muscle fibers with elevated intramyocellular Ad expression were consistently type IIA and IID fibers with detectably higher intramyocellular lipid (IMCL) content. To determine the effect of Ad on muscle phenotype and function, we used an Ad-null [knockout (KO)] mouse model. Body mass increased significantly in 24-wk-old KO mice [+5.5 ± 3% relative to wild-type mice (WT)], with no change in muscle mass observed. IMCL content was significantly increased (+75.1 ± 25%), whereas epididymal fat mass, although elevated, was not different in the KO mice compared with WT (+35.1 ± 23%; P = 0.16). Fiber-type composition was unaltered, although type IIB fiber area was increased in KO mice (+25.5 ± 6%). In situ muscle stimulation revealed lower peak tetanic forces in KO mice relative to WT (-47.5 ± 6%), with no change in low-frequency fatigue rates. These data demonstrate that the absence of Ad expression causes contractile dysfunction and phenotypical changes in skeletal muscle. Furthermore, we demonstrate that Ad is expressed in skeletal muscle and that its intramyocellular localization is associated with elevated IMCL, particularly in type IIA/D fibers. Copyright © 2008 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiologyen_HK
dc.subjectIntramyocellular lipid-
dc.subjectMuscle lipids-
dc.subjectMuscle stimulation-
dc.subjectObesity-
dc.subjectType 2 diabetes-
dc.subject.meshAdiponectin - biosynthesis - geneticsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshMuscle Fibers, Skeletal - metabolismen_HK
dc.subject.meshMuscle, Skeletal - metabolism - physiologyen_HK
dc.subject.meshPhenotypeen_HK
dc.titleAdiponectin is expressed by skeletal muscle fibers and influences muscle phenotype and functionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0363-6143&volume=295&spage=C203&epage=12&date=2008&atitle=Adiponectin+is+Expressed+by+Skeletal+Muscle+Fibers+and+Influences+Muscle+Phenotype+and+Function.en_HK
dc.identifier.emailXu, A:amxu@hkucc.hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1152/ajpcell.00030.2008en_HK
dc.identifier.pmid18463233-
dc.identifier.pmcidPMC2493546-
dc.identifier.scopuseid_2-s2.0-52749090551en_HK
dc.identifier.hkuros144264en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-52749090551&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume295en_HK
dc.identifier.issue1en_HK
dc.identifier.spageC203en_HK
dc.identifier.epageC212en_HK
dc.identifier.isiWOS:000257651700022-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridKrause, MP=15045057200en_HK
dc.identifier.scopusauthoridLiu, Y=26643544200en_HK
dc.identifier.scopusauthoridVu, V=36448715400en_HK
dc.identifier.scopusauthoridChan, L=24439401800en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridRiddell, MC=7005042076en_HK
dc.identifier.scopusauthoridSweeney, G=7102852659en_HK
dc.identifier.scopusauthoridHawke, TJ=6603394298en_HK
dc.identifier.issnl0363-6143-

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