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Eur J Clin Invest 2008; 38 (1): 71-72Editor -The presence of the metabolic syndrome (MetS) increases the risk for cardiovascular disease (CVD) and type 2 diabetes mellitus [1]. A 'new' adipocytokine named 'visfatin' (pre-B cell colony-enhancing factor) is a cytokine highly expressed in visceral fat that exhibits insulin-mimetic properties [2]. We investigated the possible differences in plasma visfatin levels between subjects with and without MetS.Consecutive patients (n = 186, 81 men/105 women) without known CVD or diabetes mellitus attending the Outpatient Lipid Clinic of the University Hospital of Ioannina participated in the present study. Ninety of them fulfilled the National Cholesterol Educational Program Adult Treatment Panel III (NCEP ATP III) criteria for the diagnosis of MetS [3] and the remaining 96 subjects served as a control group (non-MetS). Plasma visfatin concentrations were measured using an enzyme-linked immunoabsorbent assay (EIA) kit (Phoenix Pharmaceuticals, Belmont, California, USA).Plasma visfatin concentrations were higher in MetS subjects compared with non-MetS individuals [24·6 (9·1-56·6) ng mL -1 vs. 16·1 (6·7-48·7) ng mL -1 , P < 0·01], even after adjustment for age, sex and body mass index. Visfatin levels increased proportionally to the number of MetS components (P for trend < 0·01) (Fig. 1). Plasma visfatin concentrations were correlated with waist circumference (rho = 0·3, P < 0·001), triglycerides (rho = 0·35, P < 0·001), systolic (rho = 0·28, P < 0·001) and diastolic (rho = 0·27, P < 0·001) blood pressure but not with high-density lipoprotein cholesterol levels. Plasma visfatin levels were marginally correlated with fasting glucose (rho = 0·144, P = 0·055) and insulin levels (rho 0·165, P = 0·035), as well as with the homeostasis model assessment (HOMA) index (rho = 0·16, P = 0·041).In conclusion, plasma visfatin levels are increased in patients with MetS compared with individuals that do not fulfil the criteria for this syndrome. Visfatin concentrations elevate in parallel with the number of MetS components. Gene expression of visfatin was recently found to be enhanced in macrophages of human unstable carotid and coronary atherosclerotic lesions; this finding suggests a potential role for visfatin as an inflammatory mediator and in plaque destabilisation process [4]. Larger clinical studies are needed in order to assess if the observed increase in visfatin levels in MetS subjects is a consequence of the involvement of the molecule in the pathogenesis of this syndrome, or it is just an epiphenomenon that might be a useful marker of abdominal fat deposition and cardiovascular risk. Figure 1 Plasma visfatin concentrations (logarithmically transformed) in subjects with a different number of components of the metabolic syndrome (MetS). The groups consist of: MetS components = 0 n = 34 patients MetS components = 1 n = 29 patients MetS components = 2 n = 38 patients MetS components = 3 n = 50 patients MetS components = 4 n = 24 patients MetS components = 5 n = 11 patients.

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Patients with metabolic syndrome (MetS) usually have low high density lipoprotein cholesterol (HDL-C) levels. We determined the HDL distribution profile as well as the HDL-related lipoprotein associated phospholipase A(2) (HDL-LpPLA(2)) and paraoxonase-1 (PON1) activities in subjects with MetS (n = 189) but otherwise healthy. Age and sex-matched individuals (n = 166) without MetS served as controls. The lower HDL-C concentration in MetS patients was due to a reduction in both large and small HDL subclasses (P < 0.001 and P < 0.05, respectively). As the number of MetS components increased, the HDL phenotype comprised of a greater percentage of small HDL-3 and less large HDL-2 subclasses, resulting in a decreased HDL-2/HDL-3 ratio (P < 0.001 for all trends). Multivariate analysis revealed that HDL-2 levels and the HDL-2/HDL-3 ratio significantly and independently correlated with HDL-C (positively) and TG (negatively) levels. HDL-3 concentration significantly and independently positively correlated with HDL-C and TG levels. HDL-LpPLA(2) activity was decreased in MetS patients (P < 0.01), a phenomenon that may contribute to the defective antiatherogenic activity of HDL in MetS. PON1 activity did not differ between groups. We conclude that MetS, in addition to the decrease in HDL-C concentration, is associated with alterations in the HDL phenotype, which is comprised of a greater percentage of small HDL subclasses. Furthermore, HDL-LpPLA(2) activity is decreased in MetS patients.

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