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Article: Leptin and inflammation

TitleLeptin and inflammation
Authors
KeywordsAutoimmunity
Infection
Inflammation
Leptin
Issue Date2008
PublisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cir/index.htm
Citation
Current Immunology Reviews, 2008, v. 4 n. 2, p. 70-79 How to Cite?
AbstractThe past few years of research on leptin have provided important information on the link between metabolism and immune homeostasis. Adipocytes influence not only the endocrine system but also the immune response through several cytokine-like mediators known as adipokines, which include leptin. It is widely accepted that leptin can directly link nutritional status and pro-inflammatory T helper 1 immune responses, and that a decrease of leptin plasma concentration during food deprivation can lead to an impaired immune function. Additionally, several studies have implicated leptin in the pathogenesis of chronic inflammation, and the elevated circulating leptin levels in obesity appear to contribute to the low-grade inflammatory background which makes obese individuals more susceptible to increased risk of developing cardiovascular diseases, type II diabetes, or degenerative disease including autoimmunity and cancer. Conversely, reduced levels of leptin such as those found in malnourished individuals have been linked to increased risk of infection and reduced cell-mediated immune responses. We discuss here the functional influences of leptin in the physiopathology of inflammation, and the effects of leptin in the modulation of such responses. © 2008 Bentham Science Publishers Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/88287
ISSN
2015 SCImago Journal Rankings: 0.363
References

 

DC FieldValueLanguage
dc.contributor.authorIikuni, Nen_HK
dc.contributor.authorLam, QLKen_HK
dc.contributor.authorLu, Len_HK
dc.contributor.authorMatarese, Gen_HK
dc.contributor.authorLa Cava, Aen_HK
dc.date.accessioned2010-09-06T09:41:23Z-
dc.date.available2010-09-06T09:41:23Z-
dc.date.issued2008en_HK
dc.identifier.citationCurrent Immunology Reviews, 2008, v. 4 n. 2, p. 70-79en_HK
dc.identifier.issn1573-3955en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88287-
dc.description.abstractThe past few years of research on leptin have provided important information on the link between metabolism and immune homeostasis. Adipocytes influence not only the endocrine system but also the immune response through several cytokine-like mediators known as adipokines, which include leptin. It is widely accepted that leptin can directly link nutritional status and pro-inflammatory T helper 1 immune responses, and that a decrease of leptin plasma concentration during food deprivation can lead to an impaired immune function. Additionally, several studies have implicated leptin in the pathogenesis of chronic inflammation, and the elevated circulating leptin levels in obesity appear to contribute to the low-grade inflammatory background which makes obese individuals more susceptible to increased risk of developing cardiovascular diseases, type II diabetes, or degenerative disease including autoimmunity and cancer. Conversely, reduced levels of leptin such as those found in malnourished individuals have been linked to increased risk of infection and reduced cell-mediated immune responses. We discuss here the functional influences of leptin in the physiopathology of inflammation, and the effects of leptin in the modulation of such responses. © 2008 Bentham Science Publishers Ltd.en_HK
dc.languageengen_HK
dc.publisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cir/index.htmen_HK
dc.relation.ispartofCurrent Immunology Reviewsen_HK
dc.subjectAutoimmunityen_HK
dc.subjectInfectionen_HK
dc.subjectInflammationen_HK
dc.subjectLeptinen_HK
dc.titleLeptin and inflammationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1573-3955&volume=4&spage=70&epage=79&date=2008&atitle=Leptin+and+inflammation.+en_HK
dc.identifier.emailLam, QLK: qlam@pathology.hku.hken_HK
dc.identifier.emailLu, L: liweilu@hkucc.hku.hken_HK
dc.identifier.authorityLam, QLK=rp00312en_HK
dc.identifier.authorityLu, L=rp00477en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2174/157339508784325046en_HK
dc.identifier.scopuseid_2-s2.0-48249095575en_HK
dc.identifier.hkuros148788en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-48249095575&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue2en_HK
dc.identifier.spage70en_HK
dc.identifier.epage79en_HK
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridIikuni, N=10042336800en_HK
dc.identifier.scopusauthoridLam, QLK=8722491000en_HK
dc.identifier.scopusauthoridLu, L=7403963552en_HK
dc.identifier.scopusauthoridMatarese, G=7003362041en_HK
dc.identifier.scopusauthoridLa Cava, A=6701757340en_HK
dc.identifier.citeulike2781974-

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