Efficacy of antioxidant treatment in reducing resistin serum levels: A randomized study

Abstract

Objectives: Few in vitro studies have examined the participation of resistin, a recently discovered adipokine, in oxidative processes. We investigated whether in vivo treatment with the antioxidant vitamin C might affect resistin serum levels. Design: Randomized prospective open trial. Setting: San Giovanni Battista Hospital, Turin, Italy. Participants: Eighty healthy individuals. Intervention: Administration of 2 g of ascorbic acid orally for 2 wk (n = 40, experimental group) or no supplementation (n = 40; control group). Outcome measures: The primary end point was the between-group difference in the before-after change in resistin serum level after vitamin C supplementation. Secondary endpoints were the within- and between-group changes in glucose, insulin, lipid parameters, C-reactive protein fasting values, and markers of oxidative stress. Results: In the experimental group, vitamin C supplementation was significantly associated with both resistin concentration reduction (from 4.3 ± 1.5 to 2.9 ± 0.8 ng/ml; 95% confidence interval [CI] -1.87, -1.03) and ascorbic acid level increase (from 9.4 ± 2.9 to 19.0 ±,5.2 mg/l; 95% Cl 7.9, 11.2). In the control group, resistin levels did not change significantly, (from 4.2 ± 1.0 to 4.3 ± 0.9 ng/ml; 95% Cl -0.07, 0.37). The between-group differences were highly significant (p < 0.001). Vitamin C supplementation was also associated with a statistically significant reduction in nitrotyrosine level and incremental increase in reduced glutathione. In a linear regression model, within-individual changes in vitamin C concentrations were inversely correlated with changes in resistin levels in both groups (each unit increase of vitamin C corresponded to a decrease of about 0.10 units of resistin levels (95% Cl 0.13, 0.08; p < 0.001). Conclusion: This is to our knowledge the first randomized trial in humans that has demonstrated that short-term vitamin C supplementation could significantly reduce resistin levels, independent of changes in inflammatory or metabolic variables. Future investigations of resistin participation in oxidative processes are warranted.