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Article: Emerging clinical and experimental evidence for the role of lipocalin-2 in metabolic syndrome

TitleEmerging clinical and experimental evidence for the role of lipocalin-2 in metabolic syndrome
Authors
Issue Date2012
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEP
Citation
Clinical and Experimental Pharmacology & Physiology, 2012, v. 39 n. 2, p. 194-199 How to Cite?
Abstract
The inflammatory state, which is associated with the current pandemic of obesity, has been established as an important contributing pathogenic factor to the increased prevalence of the so-called metabolic syndrome. Many studies have focused on the contribution of various adipokines to this phenomenon, and in the present study, we provide an update on the emerging evidence that the pro-inflammatory factor, lipocalin-2, might influence various aspects of metabolic syndrome. Previous reports indicate a positive correlation of serum lipocalin-2 with fasting glucose, the homeostasis model assessment of insulin resistance index, and the inflammatory marker high-sensitivity C-reactive protein, even after adjustment for body mass index, suggesting that it is an independent risk factor for insulin resistance, diabetes, and inflammation. Direct analysis of lipocalin-2 action now also shows effects on peripheral metabolism and on cardiovascular function. A better understanding of how lipocalin-2 is regulated locally and systemically is crucial for adding to our understanding of the pathogenesis of metabolic syndrome, and to uncover potential new avenues for therapeutic approaches.
Persistent Identifierhttp://hdl.handle.net/10722/139606
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJang, Yen_US
dc.contributor.authorLee, JHen_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorSweeney, Gen_US
dc.date.accessioned2011-09-23T05:52:28Z-
dc.date.available2011-09-23T05:52:28Z-
dc.date.issued2012en_US
dc.identifier.citationClinical and Experimental Pharmacology & Physiology, 2012, v. 39 n. 2, p. 194-199en_US
dc.identifier.issn0305-1870-
dc.identifier.urihttp://hdl.handle.net/10722/139606-
dc.description.abstractThe inflammatory state, which is associated with the current pandemic of obesity, has been established as an important contributing pathogenic factor to the increased prevalence of the so-called metabolic syndrome. Many studies have focused on the contribution of various adipokines to this phenomenon, and in the present study, we provide an update on the emerging evidence that the pro-inflammatory factor, lipocalin-2, might influence various aspects of metabolic syndrome. Previous reports indicate a positive correlation of serum lipocalin-2 with fasting glucose, the homeostasis model assessment of insulin resistance index, and the inflammatory marker high-sensitivity C-reactive protein, even after adjustment for body mass index, suggesting that it is an independent risk factor for insulin resistance, diabetes, and inflammation. Direct analysis of lipocalin-2 action now also shows effects on peripheral metabolism and on cardiovascular function. A better understanding of how lipocalin-2 is regulated locally and systemically is crucial for adding to our understanding of the pathogenesis of metabolic syndrome, and to uncover potential new avenues for therapeutic approaches.-
dc.languageengen_US
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEP-
dc.relation.ispartofClinical and Experimental Pharmacology & Physiologyen_US
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.subject.meshAcute-Phase Proteins - physiology-
dc.subject.meshLipocalins - physiology-
dc.subject.meshMetabolic Syndrome X - metabolism - therapy-
dc.subject.meshObesity - metabolism - therapy-
dc.subject.meshProto-Oncogene Proteins - physiology-
dc.titleEmerging clinical and experimental evidence for the role of lipocalin-2 in metabolic syndromeen_US
dc.typeArticleen_US
dc.identifier.emailWang, Y: yuwanghk@hku.hken_US
dc.identifier.authorityWang, Y=rp00239en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/j.1440-1681.2011.05557.x-
dc.identifier.pmid21689137-
dc.identifier.scopuseid_2-s2.0-84863030946-
dc.identifier.hkuros195689en_US
dc.identifier.hkuros219905-
dc.identifier.volume39-
dc.identifier.issue2-
dc.identifier.spage194-
dc.identifier.epage199-
dc.identifier.isiWOS:000299618600011-
dc.publisher.placeAustralia-

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