Vol 69, No 8 (2011)
Original articles
Published online: 2011-08-17
Plasma visfatin and tumor niecross factor-alpha (TNF-α) levels in metabolic syndrome
DOI: 10.33963/v.kp.79208
Kardiol Pol 2011;69(8):802-807.
Abstract
Background: Experimental studies have shown that tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) downregulate
visfatin gene expression in adipocytes. On the other hand, the induction of cytokine production by visfatin in leucocytes
and monocytes has also been described.
Aim: To assess the possible interrelation between plasma concentrations of visfatin and TNF-α and TNF soluble receptor in obese women fulfilling, or not, the criteria of metabolic syndrome (MS).
Methods: Ninety two obese women were included in the study. Metabolic syndrome, based on IDF criteria (2005) was diagnosed in 71 subjects (mean age 53 ± 9 years; body mass index 39.1 ± 5.6 kg/m2, waist circumference 109.6 ± 11.4 cm). The remaining 21 formed the non-MS subgroup (mean age 52 ± 9 years, body mass index 36.3 ± 5.2 kg/m2, waist circumference 104.7 ± 11.0 cm). Fourteen healthy normal weight women served as controls. In all subjects, body composition was assessed by the bioimpedance method.
Results: In the MS subgroup, but not in the non-MS subgroup, visfatin levels were significantly higher than in controls. We did not observe any significant difference in plasma concentrations of visfatin, TNF-α or sTNFRs between the MS subgroup and the non-MS subgroup. Only in the MS subgroup and in the combined analysis of all study subgroups did plasma visfatin concentrations correlate significantly with TNF-α levels (R = 0.31, p = 0.01, R = 0.21, p = 0.03; respectively). Additionally, in the MS subgroup there was a positive correlation between visfatin levels and insulin resistance (R = 0.53, p = 0.01).
Conclusions: Our findings suggest that visfatin in metabolic syndrome should be regarded as a proinflammatory factor indirectly favouring the development of insulin resistance.
Kardiol Pol 2011; 69, 8: 802–807
Aim: To assess the possible interrelation between plasma concentrations of visfatin and TNF-α and TNF soluble receptor in obese women fulfilling, or not, the criteria of metabolic syndrome (MS).
Methods: Ninety two obese women were included in the study. Metabolic syndrome, based on IDF criteria (2005) was diagnosed in 71 subjects (mean age 53 ± 9 years; body mass index 39.1 ± 5.6 kg/m2, waist circumference 109.6 ± 11.4 cm). The remaining 21 formed the non-MS subgroup (mean age 52 ± 9 years, body mass index 36.3 ± 5.2 kg/m2, waist circumference 104.7 ± 11.0 cm). Fourteen healthy normal weight women served as controls. In all subjects, body composition was assessed by the bioimpedance method.
Results: In the MS subgroup, but not in the non-MS subgroup, visfatin levels were significantly higher than in controls. We did not observe any significant difference in plasma concentrations of visfatin, TNF-α or sTNFRs between the MS subgroup and the non-MS subgroup. Only in the MS subgroup and in the combined analysis of all study subgroups did plasma visfatin concentrations correlate significantly with TNF-α levels (R = 0.31, p = 0.01, R = 0.21, p = 0.03; respectively). Additionally, in the MS subgroup there was a positive correlation between visfatin levels and insulin resistance (R = 0.53, p = 0.01).
Conclusions: Our findings suggest that visfatin in metabolic syndrome should be regarded as a proinflammatory factor indirectly favouring the development of insulin resistance.
Kardiol Pol 2011; 69, 8: 802–807
Keywords: visfatinTNF-αsTNFRsobesitymetabolic syndrome
