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Article: Adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetic mice

TitleAdiponectin is required for PPARγ-mediated improvement of endothelial function in diabetic mice
Authors
Issue Date2011
PublisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/cellmet
Citation
Cell Metabolism, 2011, v. 14 n. 1, p. 104-115 How to Cite?
AbstractRosiglitazone is a PPARγ agonist commonly used to treat diabetes. In addition to improving insulin sensitivity, rosiglitazone restores normal vascular function by a mechanism that remains poorly understood. Here we show that adiponectin is required to mediate the PPARγ effect on vascular endothelium of diabetic mice. In db/db and diet-induced obese mice, PPARγ activation by rosiglitazone restores endothelium-dependent relaxation of aortae, whereas diabetic mice lacking adiponectin or treated with an anti-adiponectin antibody do not respond. Rosiglitazone stimulates adiponectin release from fat explants, and subcutaneous fat transplantation from rosiglitazone-treated mice recapitulates vasodilatation in untreated db/db recipients. Mechanistically, adiponectin activates AMPK/eNOS and cAMP/PKA signaling pathways in aortae, which increase NO bioavailability and reduce oxidative stress. Taken together, these results demonstrate that adipocyte-derived adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetes. Thus, the adipose tissue represents a promising target for treating diabetic vasculopathy. © 2011 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/135353
ISSN
2015 Impact Factor: 17.303
2015 SCImago Journal Rankings: 11.842
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grant Council4653/08M
466110
HKU 2/07C
HKU4/CRF10
CUHK
CUHK Li Ka Shing Institute of Health Sciences
Funding Information:

This study was supported by Hong Kong Research Grant Council (4653/08M, 466110, HKU 2/07C, and HKU4/CRF10), CUHK Focused Investment Scheme, and CUHK Li Ka Shing Institute of Health Sciences.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorWong, WTen_HK
dc.contributor.authorTian, XYen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorYu, Jen_HK
dc.contributor.authorLau, CWen_HK
dc.contributor.authorHoo, RLCen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorLee, VWYen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorHuang, Yen_HK
dc.date.accessioned2011-07-27T01:34:00Z-
dc.date.available2011-07-27T01:34:00Z-
dc.date.issued2011en_HK
dc.identifier.citationCell Metabolism, 2011, v. 14 n. 1, p. 104-115en_HK
dc.identifier.issn1550-4131en_HK
dc.identifier.urihttp://hdl.handle.net/10722/135353-
dc.description.abstractRosiglitazone is a PPARγ agonist commonly used to treat diabetes. In addition to improving insulin sensitivity, rosiglitazone restores normal vascular function by a mechanism that remains poorly understood. Here we show that adiponectin is required to mediate the PPARγ effect on vascular endothelium of diabetic mice. In db/db and diet-induced obese mice, PPARγ activation by rosiglitazone restores endothelium-dependent relaxation of aortae, whereas diabetic mice lacking adiponectin or treated with an anti-adiponectin antibody do not respond. Rosiglitazone stimulates adiponectin release from fat explants, and subcutaneous fat transplantation from rosiglitazone-treated mice recapitulates vasodilatation in untreated db/db recipients. Mechanistically, adiponectin activates AMPK/eNOS and cAMP/PKA signaling pathways in aortae, which increase NO bioavailability and reduce oxidative stress. Taken together, these results demonstrate that adipocyte-derived adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetes. Thus, the adipose tissue represents a promising target for treating diabetic vasculopathy. © 2011 Elsevier Inc.en_HK
dc.languageengen_US
dc.publisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/cellmeten_HK
dc.relation.ispartofCell Metabolismen_HK
dc.subject.meshAMP-Activated Protein Kinases - metabolism-
dc.subject.meshAdiponectin - metabolism-
dc.subject.meshDiabetes Mellitus, Experimental - drug therapy - metabolism-
dc.subject.meshEndothelium, Vascular - drug effects - metabolism - physiology-
dc.subject.meshPPAR gamma - agonists - metabolism-
dc.titleAdiponectin is required for PPARγ-mediated improvement of endothelial function in diabetic miceen_HK
dc.typeArticleen_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailHoo, RLC: rubyhoo@hkucc.hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.identifier.authorityHoo, RLC=rp01334en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cmet.2011.05.009en_HK
dc.identifier.pmid21723508-
dc.identifier.scopuseid_2-s2.0-79960018147en_HK
dc.identifier.hkuros187486en_US
dc.identifier.hkuros204664-
dc.identifier.hkuros226362-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79960018147&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issue1en_HK
dc.identifier.spage104en_HK
dc.identifier.epage115en_HK
dc.identifier.isiWOS:000292583200013-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectVascular dysfunction in obesity and diabetes: from risk prediction to therapeutic intervention-
dc.identifier.scopusauthoridWong, WT=35932584500en_HK
dc.identifier.scopusauthoridTian, XY=35768379500en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridYu, J=35351306800en_HK
dc.identifier.scopusauthoridLau, CW=7401968520en_HK
dc.identifier.scopusauthoridHoo, RLC=6602369766en_HK
dc.identifier.scopusauthoridWang, Y=7601489381en_HK
dc.identifier.scopusauthoridLee, VWY=7402507380en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridHuang, Y=34770945300en_HK

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