OBJECTIVE: The discovery of visfatin has great potential to significantly enhance our understanding of impaired fasting glucose and diabetes mellitus. The aim of the present study was to explore the relation of visfatin concentrations to cardiovascular risk factors and serum adipocytokine concentrations in patients with impaired fasting glucose. METHODS: A sample of 55 patients with impaired fasting glucose was analyzed in a prospective way. All patients with a 2-wk weight-stabilization period before recruitment were enrolled. Weight, blood pressure, basal glucose, lipoprotein(a), C-reactive protein, insulin, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triacylglycerols, blood, and adipocytokines (visfatin, leptin, adiponectin, resistin, tumor necrosis factor-α [TNF-α], and interleukin-6) levels were measured. Tetrapolar impedancometry, indirect calorimetry, and prospective serial assessment of nutritional intake with 3-d written food records were performed. RESULTS: Fourteen men (25.5%) and 41 women (74.5%), with a mean age of 57.3 ± 11.7 y and mean body mass index of 35.8 ± 3.6 kg/m(2), were included. Patients were divided in two groups by median visfatin value (18.2 ng/mL): group I had low values and group II had high values. Patients in group I had greater weight, body mass index, fat mass, fat-free mass, and adiponectin than patients in group II. Patients in group II had higher total cholesterol, low-density lipoprotein cholesterol, resistin, and TNF-α levels than patients in group I. In the multivariate analysis with age- and sex-adjusted basal visfatin concentration as a dependent variable, only TNF-α remained an independent predictor in the model (F = 8.4, P < 0.05), with an inverse correlation. Visfatin concentration decreased 7.33 ng/mL (95% confidence interval 2.10-12.58) for each nanogram per milligram of TNF-α increase. CONCLUSION: Only TNF-α is related in an independent way to serum visfatin levels.
OBJECTIVE: The discovery of visfatin has great potential to significantly enhance our understanding of impaired fasting glucose and diabetes mellitus. The aim of the present study was to explore the relation of visfatin concentrations to cardiovascular risk factors and serum adipocytokine concentrations in patients with impaired fasting glucose. METHODS: A sample of 55 patients with impaired fasting glucose was analyzed in a prospective way. All patients with a 2-wk weight-stabilization period before recruitment were enrolled. Weight, blood pressure, basal glucose, lipoprotein(a), C-reactive protein, insulin, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triacylglycerols, blood, and adipocytokines (visfatin, leptin, adiponectin, resistin, tumor necrosis factor-α [TNF-α], and interleukin-6) levels were measured. Tetrapolar impedancometry, indirect calorimetry, and prospective serial assessment of nutritional intake with 3-d written food records were performed. RESULTS: Fourteen men (25.5%) and 41 women (74.5%), with a mean age of 57.3 ± 11.7 y and mean body mass index of 35.8 ± 3.6 kg/m(2), were included. Patients were divided in two groups by median visfatin value (18.2 ng/mL): group I had low values and group II had high values. Patients in group I had greater weight, body mass index, fat mass, fat-free mass, and adiponectin than patients in group II. Patients in group II had higher total cholesterol, low-density lipoprotein cholesterol, resistin, and TNF-α levels than patients in group I. In the multivariate analysis with age- and sex-adjusted basal visfatin concentration as a dependent variable, only TNF-α remained an independent predictor in the model (F = 8.4, P < 0.05), with an inverse correlation. Visfatin concentration decreased 7.33 ng/mL (95% confidence interval 2.10-12.58) for each nanogram per milligram of TNF-α increase. CONCLUSION: Only TNF-α is related in an independent way to serum visfatin levels.