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

Krisztián Vörös, L. Gráf, Z. Prohászka, László Gráf, Péter Szenthe, Edit Kaszás, Zoltán Böröcz, K. Cseh, L. Kalabay

Research output: Contribution to journalArticle

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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-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 2011

Fingerprint

alpha-2-HS-Glycoprotein
Resistin
Adiponectin
Metabolic Networks and Pathways
Adipokines
Tumor Necrosis Factor-alpha
Myocardial Infarction
Leptin
C-Reactive Protein
Glycoproteins
Serum
Atherosclerosis
Inflammation
Insulin
Immunodiffusion
Adipocytes
Coronary Disease
Insulin Resistance
Obesity
Cross-Sectional Studies

Keywords

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

ASJC Scopus subject areas

  • Medicine(all)
  • Clinical Biochemistry
  • Biochemistry

Cite this

Serum fetuin-A in metabolic and inflammatory pathways in patients with myocardial infarction. / Vörös, Krisztián; Gráf, L.; Prohászka, Z.; Gráf, László; Szenthe, Péter; Kaszás, Edit; Böröcz, Zoltán; Cseh, K.; Kalabay, L.

In: European Journal of Clinical Investigation, Vol. 41, No. 7, 07.2011, p. 703-709.

Research output: Contribution to journalArticle

Vörös, Krisztián ; Gráf, L. ; Prohászka, Z. ; Gráf, László ; Szenthe, Péter ; Kaszás, Edit ; Böröcz, Zoltán ; Cseh, K. ; Kalabay, L. / Serum fetuin-A in metabolic and inflammatory pathways in patients with myocardial infarction. In: European Journal of Clinical Investigation. 2011 ; Vol. 41, No. 7. pp. 703-709.
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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-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.",
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AU - Vörös, Krisztián

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AU - Prohászka, Z.

AU - Gráf, László

AU - Szenthe, Péter

AU - Kaszás, Edit

AU - Böröcz, Zoltán

AU - Cseh, K.

AU - Kalabay, L.

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N2 - 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-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.

AB - 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-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.

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KW - Resistin

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