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dc.contributor.authorVural, Burçak
dc.contributor.authorAtalar, Fatmahan
dc.contributor.authorÇiftçi, Çavlan
dc.contributor.authorDemirkan, Ayşe
dc.contributor.authorSüsleyici-Duman, Belgin
dc.contributor.authorGünay, Demet
dc.contributor.authorBüyükdevrim, Ahmet Sevim
dc.date.accessioned2014-10-15T11:34:05Z
dc.date.available2014-10-15T11:34:05Z
dc.date.issued2008
dc.identifier.citationVural B, Atalar F, Ciftci C, Demirkan A, Susleyici-Duman B, Gunay D, Akpinar B, Sagbas E, Ozbek U, Buyukdevrim AS. Presence of fatty-acid-binding protein 4 expression in human epicardial adipose tissue in metabolic syndrome. Cardiovascular Pathology. 2008;17(6): 392-8. doi: 10.1016/j.carpath.2008.02.006.en_US
dc.identifier.issn1054-8807
dc.identifier.urihttp://hdl.handle.net/11446/461en_US
dc.identifier.urihttp://www.journals.elsevier.com/cardiovascular-pathology/en_US
dc.identifier.urihttp://hdl.handle.net/11446/461en_US
dc.descriptionİstanbul Bilim Üniversitesi, Tıp Fakültesi.en_US
dc.description.abstractBackground: Metabolic syndrome is a cluster of different clinical manifestations that are risk factors for atherothrombotic cardiovascular disorders. Fatty-acid-binding protein 4 (FABP4/aP2), which is highly expressed in adipocytes, specifically exerts intracellular lipid trafficking. A high level of fatty-acid-binding protein 4 expression present in obese subjects has also been found in mice and humans, especially in macrophages at atherosclerotic lesions. An in vivo study demonstrated that the inhibitor of aP2 would be a new therapeutic agent for treating metabolic diseases in mice. We have investigated the mRNA expression of fatty-acid-binding protein 4 in human epicardial adipose and ascending aorta tissues of metabolic syndrome and nonmetabolic syndrome patients. Methods: Paired epicardial adipose and ascending aorta tissue samples were obtained from 10 metabolic syndrome patients and 4 nonmetabolic syndrome patients during coronary bypass grafting and aortic valve replacement therapy, respectively. Fatty-acid-binding protein 4 gene expression was determined by quantitative real-time polymerase chain reaction. Results and Conclusions: Fatty-acid-binding protein 4 expression of epicardial adipose tissue was significantly higher in metabolic syndrome patients than in nonmetabolic syndrome controls (Pb.05). In metabolic syndrome patients, fatty-acid-binding protein 4 expression in epicardial adipose tissue was 66 times higher than fatty-acid-binding protein 4 expression in ascending aorta tissue. The expression level of fatty-acid-binding protein 4 in epicardial adipose tissue was found to be significantly correlated with waist circumference in all subjects (r=.535, Pb.05). Our data showed for the first time that human epicardial adipose and ascending aorta tissues express fatty-acid-binding protein 4 and that its level of expression in epicardial adipose tissues of metabolic syndrome patients is elevated. Increased fatty-acid-binding protein 4 gene expression in epicardial adipose tissues of metabolic syndrome patients led us think that fatty-acid-binding protein 4 might be an important factor in metabolic syndrome.en_US
dc.description.urihttp://ac.els-cdn.com/S1054880708000343/1-s2.0-S1054880708000343-main.pdf?_tid=ede7ad9a-545c-11e4-9267-00000aab0f6b&acdnat=1413372063_d79f2de0b0fe81ba12e44f93bd231d32en_US
dc.language.isoengen_US
dc.publisherElsevieren_US
dc.relation.ispartofseriesCardiovascular Pathologyen_US
dc.rightsinfo:eu-repo/semantics/embargoedAccessen_US
dc.subjectascending aortaen_US
dc.subjectepicardial adipose tissueen_US
dc.subjectFABP4en_US
dc.subjectmetabolic syndromeen_US
dc.titlePresence of fatty-acid-binding protein 4 expression in human epicardial adipose tissue in metabolic syndromeen_US
dc.typearticleen_US
dc.contributor.departmentDBÜ, Tıp Fakültesien_US
dc.identifier.issue6
dc.identifier.volume17
dc.identifier.startpage392
dc.identifier.endpage398
dc.contributor.authorIDTR167368en_US
dc.contributor.authorIDTR115014en_US
dc.contributor.authorIDTR9812en_US
dc.contributor.authorIDTR140965en_US
dc.contributor.authorIDTR136942en_US
dc.contributor.authorIDTR167476en_US
dc.relation.publicationcategoryBelirsizen_US


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