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Article: Hyperglycemia- and hyperinsulinemia-induced alteration of adiponectin receptor expression and adiponectin effects in L6 myoblasts

TitleHyperglycemia- and hyperinsulinemia-induced alteration of adiponectin receptor expression and adiponectin effects in L6 myoblasts
Authors
Issue Date2005
PublisherSociety for Endocrinology. The Journal's web site is located at http://jme.endocrinology-journals.org/
Citation
Journal Of Molecular Endocrinology, 2005, v. 35 n. 3, p. 465-476 How to Cite?
AbstractAdiponectin has been shown to regulate glucose and fatty acid uptake and metabolism in skeletal muscle. Here we investigated the role of the recently cloned adiponectin receptor (AdipoR) isoforms in mediating effects of both globular (gAd) and full-length (fAd) adiponectin, and their regulation by hyperglycemia (25 mM, 20 h) and hyperinsulinemia (100 nM, 20 h). We used L6 rat skeletal muscle cells, which were found to express both AdipoR1 and AdipoR2 mRNA in a ratio of over 6:1 respectively. Hyperglycemia and hyperinsulinemia both decreased AdipoR1 receptor expression by approximately 50%, while the latter induced an increase of approximately threefold in AdipoR2 expression. The ability of gAd to increase GLUT4 myc translocation, glucose uptake, fatty acid uptake and oxidation, as well as AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) phosphorylation, was decreased by both hyperglycemia and hyperinsulinemia. Interestingly, hyperinsulinemia induced the ability of fAd to elicit fatty acid uptake and enhanced fatty acid oxidation in response to fAd. In summary, our results suggest that both hyperglycemia and hyperinsulinemia cause gAd resistance in rat skeletal muscle cells. However, hyperinsulinemia induces a switch toward increased fAd sensitivity in these cells. © 2005 Society for Endocrinology.
Persistent Identifierhttp://hdl.handle.net/10722/78449
ISSN
2015 Impact Factor: 2.947
2015 SCImago Journal Rankings: 1.674
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFang, Xen_HK
dc.contributor.authorPalanivel, Ren_HK
dc.contributor.authorZhou, Xen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorSweeney, Gen_HK
dc.date.accessioned2010-09-06T07:43:01Z-
dc.date.available2010-09-06T07:43:01Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Molecular Endocrinology, 2005, v. 35 n. 3, p. 465-476en_HK
dc.identifier.issn0952-5041en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78449-
dc.description.abstractAdiponectin has been shown to regulate glucose and fatty acid uptake and metabolism in skeletal muscle. Here we investigated the role of the recently cloned adiponectin receptor (AdipoR) isoforms in mediating effects of both globular (gAd) and full-length (fAd) adiponectin, and their regulation by hyperglycemia (25 mM, 20 h) and hyperinsulinemia (100 nM, 20 h). We used L6 rat skeletal muscle cells, which were found to express both AdipoR1 and AdipoR2 mRNA in a ratio of over 6:1 respectively. Hyperglycemia and hyperinsulinemia both decreased AdipoR1 receptor expression by approximately 50%, while the latter induced an increase of approximately threefold in AdipoR2 expression. The ability of gAd to increase GLUT4 myc translocation, glucose uptake, fatty acid uptake and oxidation, as well as AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) phosphorylation, was decreased by both hyperglycemia and hyperinsulinemia. Interestingly, hyperinsulinemia induced the ability of fAd to elicit fatty acid uptake and enhanced fatty acid oxidation in response to fAd. In summary, our results suggest that both hyperglycemia and hyperinsulinemia cause gAd resistance in rat skeletal muscle cells. However, hyperinsulinemia induces a switch toward increased fAd sensitivity in these cells. © 2005 Society for Endocrinology.en_HK
dc.languageengen_HK
dc.publisherSociety for Endocrinology. The Journal's web site is located at http://jme.endocrinology-journals.org/en_HK
dc.relation.ispartofJournal of Molecular Endocrinologyen_HK
dc.rightsJournal of Molecular Endocrinology. Copyright © Society for Endocrinology.en_HK
dc.subject.meshAMP-Activated Protein Kinasesen_HK
dc.subject.meshAcetyl-CoA Carboxylase - metabolismen_HK
dc.subject.meshAdiponectin - chemistry - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshBiological Transport, Active - drug effectsen_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshDNA, Complementary - geneticsen_HK
dc.subject.meshFatty Acids - metabolismen_HK
dc.subject.meshGene Expression - drug effectsen_HK
dc.subject.meshGlucose - metabolismen_HK
dc.subject.meshGlucose Transporter Type 4 - metabolismen_HK
dc.subject.meshHyperglycemia - genetics - metabolismen_HK
dc.subject.meshHyperinsulinism - genetics - metabolismen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMultienzyme Complexes - metabolismen_HK
dc.subject.meshMyoblasts, Skeletal - drug effects - metabolismen_HK
dc.subject.meshOxidation-Reductionen_HK
dc.subject.meshProtein-Serine-Threonine Kinases - metabolismen_HK
dc.subject.meshRatsen_HK
dc.subject.meshReceptors, Adiponectinen_HK
dc.subject.meshReceptors, Cell Surface - geneticsen_HK
dc.subject.meshRecombinant Proteins - chemistry - pharmacologyen_HK
dc.titleHyperglycemia- and hyperinsulinemia-induced alteration of adiponectin receptor expression and adiponectin effects in L6 myoblastsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0952-5041&volume=35&spage=465&epage=76&date=2005&atitle=Hyperglycemia-+And+Hyperinsulinemia-induced+Alteration+Of+Adiponectin+Receptor+Expression+And+Adiponectin+Effects+In+L6+Myoblasts.en_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1677/jme.1.01877en_HK
dc.identifier.pmid16326833-
dc.identifier.scopuseid_2-s2.0-29744437890en_HK
dc.identifier.hkuros113388en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-29744437890&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume35en_HK
dc.identifier.issue3en_HK
dc.identifier.spage465en_HK
dc.identifier.epage476en_HK
dc.identifier.isiWOS:000234210100005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridFang, X=10642149900en_HK
dc.identifier.scopusauthoridPalanivel, R=8655817100en_HK
dc.identifier.scopusauthoridZhou, X=7410094377en_HK
dc.identifier.scopusauthoridLiu, Y=26643544200en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridSweeney, G=7102852659en_HK

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