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Article: Signaling mechanisms underlying the insulin-sensitizing effects of adiponectin

TitleSignaling mechanisms underlying the insulin-sensitizing effects of adiponectin
Authors
Issue Date2014
PublisherBailliere Tindall. The Journal's web site is located at http://www.elsevier.com/locate/beem
Citation
Best Practice & Research: Clinical Endocrinology & Metabolism, 2014, v. 28 n. 1, p. 3-13 How to Cite?
AbstractAdiponectin is an insulin-sensitizing adipokine with protective effects against a cluster of obesity-related metabolic and cardiovascular disorders. The adipokine exerts its insulin-sensitizing effects by alleviation of obesity-induced ectopic lipid accumulation, lipotoxicity and chronic inflammation, as well as by direct cross-talk with insulin signaling cascades. Adiponectin and insulin signaling pathways converge at the adaptor protein APPL1. On the one hand, APPL1 interacts with adiponectin receptors and mediates both metabolic and vascular actions of adiponectin through activation of AMP-activated protein kinase and p38 MAP kinase. On the other hand, APPL1 potentiates both the actions and secretion of insulin by fine-tuning the Akt activity in multiple insulin target tissues. In obese animals, reduced APPL1 expression contributes to both insulin resistance and defective insulin secretion. This review summarizes recent advances on the molecular mechanisms by which adiponectin sensitizes insulin actions, and discusses the roles of APPL1 in regulating both adiponectin and insulin signaling cascades.
Persistent Identifierhttp://hdl.handle.net/10722/189276
ISSN
2015 Impact Factor: 5.07
2015 SCImago Journal Rankings: 2.183
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCheng, KYen_US
dc.contributor.authorLam, KSLen_US
dc.contributor.authorWang, Ben_US
dc.contributor.authorXu, Aen_US
dc.date.accessioned2013-09-17T14:31:13Z-
dc.date.available2013-09-17T14:31:13Z-
dc.date.issued2014en_US
dc.identifier.citationBest Practice & Research: Clinical Endocrinology & Metabolism, 2014, v. 28 n. 1, p. 3-13en_US
dc.identifier.issn1521-690X-
dc.identifier.urihttp://hdl.handle.net/10722/189276-
dc.description.abstractAdiponectin is an insulin-sensitizing adipokine with protective effects against a cluster of obesity-related metabolic and cardiovascular disorders. The adipokine exerts its insulin-sensitizing effects by alleviation of obesity-induced ectopic lipid accumulation, lipotoxicity and chronic inflammation, as well as by direct cross-talk with insulin signaling cascades. Adiponectin and insulin signaling pathways converge at the adaptor protein APPL1. On the one hand, APPL1 interacts with adiponectin receptors and mediates both metabolic and vascular actions of adiponectin through activation of AMP-activated protein kinase and p38 MAP kinase. On the other hand, APPL1 potentiates both the actions and secretion of insulin by fine-tuning the Akt activity in multiple insulin target tissues. In obese animals, reduced APPL1 expression contributes to both insulin resistance and defective insulin secretion. This review summarizes recent advances on the molecular mechanisms by which adiponectin sensitizes insulin actions, and discusses the roles of APPL1 in regulating both adiponectin and insulin signaling cascades.-
dc.languageengen_US
dc.publisherBailliere Tindall. The Journal's web site is located at http://www.elsevier.com/locate/beem-
dc.relation.ispartofBest Practice & Research: Clinical Endocrinology & Metabolismen_US
dc.titleSignaling mechanisms underlying the insulin-sensitizing effects of adiponectinen_US
dc.typeArticleen_US
dc.identifier.emailCheng, KY: dorncky@hkucc.hku.hken_US
dc.identifier.emailLam, KSL: ksllam@hku.hken_US
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_US
dc.identifier.authorityCheng, KY=rp01672en_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.doi10.1016/j.beem.2013.06.006-
dc.identifier.pmid24417941-
dc.identifier.hkuros225101en_US
dc.identifier.hkuros227960-
dc.identifier.volume28-
dc.identifier.issue1-
dc.identifier.spage3-
dc.identifier.epage13-
dc.identifier.isiWOS:000330817300002-
dc.publisher.placeUnited Kingdom-

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