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dc.contributor.author Vörös, Krisztián
dc.contributor.author Gráf, László Jr.
dc.contributor.author Prohászka, Zoltán
dc.contributor.author Gráf, László
dc.contributor.author Szenthe P
dc.contributor.author Kaszas E
dc.contributor.author Böröcz, Zoltán
dc.contributor.author Cseh, Károly
dc.contributor.author Kalabay, László
dc.date.accessioned 2018-10-10T08:17:19Z
dc.date.available 2018-10-10T08:17:19Z
dc.date.issued 2011
dc.identifier 79958728276
dc.identifier.citation pagination=703-709; journalVolume=41; journalIssueNumber=7; journalTitle=EUROPEAN JOURNAL OF CLINICAL INVESTIGATION;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/6365
dc.identifier.uri doi:10.1111/j.1365-2362.2010.02456.x
dc.description.abstract Eur J Clin Invest 2011 ABSTRACT: Background Although multifunctional glycoprotein alpha2HS-glycoprotein/human fetuin-A (AHSG) is involved in atherosclerosis, it is not clear whether high or low concentrations are more important. We studied the correlation of serum AHSG with adiponectin, leptin, resistin, C-reactive protein (CRP) and tumour necrosis factor-alpha (TNF-alpha) to see whether its metabolic effects or its involvement in subclinical inflammation are dominant in patients with established coronary disease. Materials and methods In this cross-sectional study, AHSG concentration was determined in sera of 171 patients (age: 62 +/- 6 years, mean +/- SD) with previous myocardial STEMI infarction and normal renal function and 81 age-matched healthy controls by radial immunodiffusion. Results Patients had increased AHSG levels (673 +/- 103 vs. 619 +/- 96 mg L(-1) , P < 0.001) compared to controls. Obese and diabetic patients had higher AHSG concentration than those with normal BMI or without diabetes but even the latter group had elevated AHSG levels (667 +/- 101 mg L(-1) , n = 88) compared to controls (P = 0.002). Serum AHSG correlated negatively with adiponectin (r = -0.236, P = 0.006) even after adjusting for BMI (r = -0.177, P = 0.043). AHSG determined adiponectin levels independently from BMI, age and other adipocytokines (P = 0.014). The correlation between leptin and AHSG (r = 0.321, P = 0.021) weakened following adjustment for BMI (r = 0.209, P = 0.072). Serum AHSG did not correlate significantly with CRP, resistin and TNF-alpha concentrations. BMI and resistin but not AHSG determined TNF-alpha levels independently. Conclusions AHSG is elevated in sera of patients with previous myocardial infarction. Association with adipokines favours the concept that AHSG is involved in atherosclerosis more likely through metabolic pathways (insulin resistance, obesity and adipocyte dysfunction) than by inflammation in patients with post-myocardial infarction.
dc.relation.ispartof urn:issn:0014-2972
dc.title Serum fetuin-A in metabolic and inflammatory pathways in patients with myocardial infarction.
dc.type Journal Article
dc.date.updated 2018-09-02T09:28:09Z
dc.language.rfc3066 en
dc.identifier.mtmt 1459007
dc.identifier.wos 000292298100002
dc.identifier.pubmed 21226708
dc.contributor.department MTA-SE Gyulladásbiológiai és Immungenomikai Kutatócsoport (2006-ig: MTA-SE Molekuláris Immunológiai Kutatócsoport) [2009.12.31]
dc.contributor.institution MTA Támogatott Kutatócsoportok


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