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Article: Leptin prevents the metabolic effects of adiponectin in L6 myotubes

TitleLeptin prevents the metabolic effects of adiponectin in L6 myotubes
Authors
Issue Date2009
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00125/index.htm
Citation
Diabetologia, 2009, v. 52 n. 10, p. 2190-2200 How to Cite?
AbstractAims/hypothesis: Adiponectin and leptin are negatively and positively correlated with human obesity respectively, and have both been shown to regulate energy metabolism in skeletal muscle. However, little is known about their signalling and functional crosstalk. Here we investigated the effects of leptin on metabolic actions of (1) globular adiponectin (gAd) and (2) full-length adiponectin (fAd) in L6 cells. Methods: Glucose uptake was measured upon gAd and fAd treatment after incubation with different doses (0.3, 0.6, 3, 6, 60 nmol/l) of leptin for 6, 12 and 24 h. We also measured adiponectin receptor (ADIPOR) expression and stimulation of downstream signalling by gAd and fAd using co-immunoprecipitation and western blotting following leptin pretreatment, as well as analysis of fatty acid uptake and oxidation using radiolabelled tracers. Results: Leptin attenuated the stimulation of glucose uptake by gAd and fAd in a dose- and time-dependent manner, a finding correlated with decreased levels of ADIPOR1 and ADIPOR2. gAd and fAd increased palmitate uptake via activation of AMP protein kinase (T172), enhanced expression of the fatty acid transporter CD36, phosphorylated acetyl-CoA carboxylase (S79) and enhanced palmitate oxidation, all of which were attenuated by leptin pretreatment. Adiponectin can also enhance insulin sensitivity via direct signalling crosstalk; here we show that enhanced insulin-stimulated IRS-1 (Y612) and Akt (T308) phosphorylation in response to fAd was attenuated by leptin. APPL1 was recently identified as a critical mediator of adiponectin action in skeletal muscle. We demonstrated that leptin attenuated binding of APPL1 to LKB1, a downstream target leading to AMPK phosphorylation. Conclusions/interpretation: The direct metabolic and insulin-sensitising effects of adiponectin were attenuated in the presence of leptin. © 2009 Springer-Verlag.
Persistent Identifierhttp://hdl.handle.net/10722/163271
ISSN
2015 Impact Factor: 6.206
2015 SCImago Journal Rankings: 3.528
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFang, Xen_US
dc.contributor.authorFetros, Jen_US
dc.contributor.authorDadson, KEen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorSweeney, Gen_US
dc.date.accessioned2012-09-05T05:29:24Z-
dc.date.available2012-09-05T05:29:24Z-
dc.date.issued2009en_US
dc.identifier.citationDiabetologia, 2009, v. 52 n. 10, p. 2190-2200en_US
dc.identifier.issn0012-186Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/163271-
dc.description.abstractAims/hypothesis: Adiponectin and leptin are negatively and positively correlated with human obesity respectively, and have both been shown to regulate energy metabolism in skeletal muscle. However, little is known about their signalling and functional crosstalk. Here we investigated the effects of leptin on metabolic actions of (1) globular adiponectin (gAd) and (2) full-length adiponectin (fAd) in L6 cells. Methods: Glucose uptake was measured upon gAd and fAd treatment after incubation with different doses (0.3, 0.6, 3, 6, 60 nmol/l) of leptin for 6, 12 and 24 h. We also measured adiponectin receptor (ADIPOR) expression and stimulation of downstream signalling by gAd and fAd using co-immunoprecipitation and western blotting following leptin pretreatment, as well as analysis of fatty acid uptake and oxidation using radiolabelled tracers. Results: Leptin attenuated the stimulation of glucose uptake by gAd and fAd in a dose- and time-dependent manner, a finding correlated with decreased levels of ADIPOR1 and ADIPOR2. gAd and fAd increased palmitate uptake via activation of AMP protein kinase (T172), enhanced expression of the fatty acid transporter CD36, phosphorylated acetyl-CoA carboxylase (S79) and enhanced palmitate oxidation, all of which were attenuated by leptin pretreatment. Adiponectin can also enhance insulin sensitivity via direct signalling crosstalk; here we show that enhanced insulin-stimulated IRS-1 (Y612) and Akt (T308) phosphorylation in response to fAd was attenuated by leptin. APPL1 was recently identified as a critical mediator of adiponectin action in skeletal muscle. We demonstrated that leptin attenuated binding of APPL1 to LKB1, a downstream target leading to AMPK phosphorylation. Conclusions/interpretation: The direct metabolic and insulin-sensitising effects of adiponectin were attenuated in the presence of leptin. © 2009 Springer-Verlag.en_US
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00125/index.htmen_US
dc.relation.ispartofDiabetologiaen_US
dc.subject.meshAdiponectin - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Transport - Drug Effectsen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCell Lineen_US
dc.subject.meshGlucose - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoprecipitationen_US
dc.subject.meshLeptin - Pharmacologyen_US
dc.subject.meshMuscle, Skeletal - Drug Effects - Metabolismen_US
dc.subject.meshRatsen_US
dc.titleLeptin prevents the metabolic effects of adiponectin in L6 myotubesen_US
dc.typeArticleen_US
dc.identifier.emailXu, A:amxu@hkucc.hku.hken_US
dc.identifier.authorityXu, A=rp00485en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s00125-009-1462-0en_US
dc.identifier.pmid19636528-
dc.identifier.scopuseid_2-s2.0-69949163645en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-69949163645&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume52en_US
dc.identifier.issue10en_US
dc.identifier.spage2190en_US
dc.identifier.epage2200en_US
dc.identifier.isiWOS:000269848100026-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridFang, X=10642149900en_US
dc.identifier.scopusauthoridFetros, J=40261265300en_US
dc.identifier.scopusauthoridDadson, KE=13204705900en_US
dc.identifier.scopusauthoridXu, A=7202655409en_US
dc.identifier.scopusauthoridSweeney, G=7102852659en_US
dc.identifier.citeulike5321677-

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