Plasma visfatin concentrations after a lifestyle intervention were directly associated with inflammatory markers

Abstract

Background and aims The biological activity and regulation of the novel adipokine visfatin are still largely unknown. Our aim was to evaluate if visfatin plasma concentrations may be influenced by a lifestyle intervention. Methods and results Out of 335 dysmetabolic patients from a population-based cohort, randomized to receive a lifestyle intervention program (intervention group) or family physician usual care (controls), 20 patients per group were randomly selected for plasma visfatin determination. The before–after variation (Δ) in visfatin concentration at 1-year from randomization, and the correlations between Δvisfatin and intervention-induced changes in waist circumference, fasting glucose, markers of inflammation, and oxidative stress were evaluated. The intervention group showed a significant improvement in waist circumference, and many metabolic/inflammatory variables, while the controls worsened. Visfatin concentrations slightly decreased in the former and significantly increased in the controls (Δvisfatin = −2.4 vs 66.0 ng/ml, p < 0.001). In robust regression models, the following variables resulted associated with Δvisfatin: Δwaist circumference, Δfasting glucose, Δhs-CRP (high-sensitivity C-reactive protein) and ΔTNFα (tumor necrosis factor-α). Significant effects on Δvisfatin of ΔTNFα ( β = 16.8; 6.1–25.6; p = 0.003) and, modified by group, of Δhs-CRP ( β = 29.8; 95% CI 15.4–44.2; p < 0.001 and β = 4.2; 2.9–5.5; p < 0.001 in the control and intervention group, respectively) were detected. By controlling for Δwaist, the effects of ΔTNFα and of Δhs-CRP on Δvisfatin by group did not change, while Δwaist was no longer associated. The association between Δvisfatin and Δglucose was no longer significant, after adjusting for Δhs-CRP. Conclusion Visfatin values increased with waist circumference and were associated with variations of inflammatory markers, suggesting participation in inflammatory mechanisms.