Serum fetuin-A in metabolic and inflammatory pathways in patients with myocardial infarction

Krisztián Vörös, László Gráf, Zoltán Prohászka, László Gráf, Péter Szenthe, Edit Kaszás, Zoltán Böröcz, Károly Cseh, László Kalabay

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Background Although multifunctional glycoprotein α2HS-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-α (TNF-α) 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±6years, 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±96mgL-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±101mgL-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-α concentrations. BMI and resistin but not AHSG determined TNF-α 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.

Original languageEnglish
Pages (from-to)703-709
Number of pages7
JournalEuropean Journal of Clinical Investigation
Volume41
Issue number7
DOIs
Publication statusPublished - Jul 1 2011

Keywords

  • Adiponectin
  • Leptin
  • Myocardial infarction
  • Resistin
  • Tumour necrosis factor-α
  • αlpha2HS-glycoprotein/fetuin-A

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry

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