BACKGROUND: Exogenous leptin markedly decreased plasma paraoxonase (PON1) activity in rats. Hyperleptinemia and decreased PON1 activity have previously been demonstrated in uremia. Therefore, we investigated the relationship between leptin level and PON1 activity in hemodialysis (HD) patients. METHODS: Leptin and PON1 were determined in 40 HD patients and 40 age-matched controls with similar body mass index (BMI). RESULTS: Leptin was higher (p < 0.001) and PON1 activity was lower (p < 0.001) in HD patients than in controls. PON1 and PON1/HDL ratio was higher in HD patients with BMI >25 kg/m2 than in HD patients with BMI <25 kg/m2. It was not due to a difference in frequency of high activity phenotype of PON1 among subgroups of HD patients. There was no similar difference in controls. Spearman analysis showed a significant correlation between leptin and PON1 activity (p < 0.02), BMI (p < 0.001), triglyceride (TG) (p < 0.03), and Kt/V (-0.323, p < 0.03), but multiparametric regression analysis did not reveal it. PON1 activity depended on BMI in both models. In controls, leptin correlated with BMI (p < 0.001) and TG (p < 0.002) but not PON1 activity. A slight decrease in leptin concentration and PON1 activity during HD was observed. CONCLUSION: Our results suggest the role of other pathophysiological conditions besides hyperleptinemia resulting in decreased PON1 activity in HD patients. Copyright 2006 S. Karger AG, Basel
BACKGROUND: Exogenous leptin markedly decreased plasma paraoxonase (PON1) activity in rats. Hyperleptinemia and decreased PON1 activity have previously been demonstrated in uremia. Therefore, we investigated the relationship between leptin level and PON1 activity in hemodialysis (HD) patients. METHODS: Leptin and PON1 were determined in 40 HDpatients and 40 age-matched controls with similar body mass index (BMI). RESULTS: Leptin was higher (p < 0.001) and PON1 activity was lower (p < 0.001) in HDpatients than in controls. PON1 and PON1/HDL ratio was higher in HDpatients with BMI >25 kg/m2 than in HDpatients with BMI <25 kg/m2. It was not due to a difference in frequency of high activity phenotype of PON1 among subgroups of HDpatients. There was no similar difference in controls. Spearman analysis showed a significant correlation between leptin and PON1 activity (p < 0.02), BMI (p < 0.001), triglyceride (TG) (p < 0.03), and Kt/V (-0.323, p < 0.03), but multiparametric regression analysis did not reveal it. PON1 activity depended on BMI in both models. In controls, leptin correlated with BMI (p < 0.001) and TG (p < 0.002) but not PON1 activity. A slight decrease in leptin concentration and PON1 activity during HD was observed. CONCLUSION: Our results suggest the role of other pathophysiological conditions besides hyperleptinemia resulting in decreased PON1 activity in HDpatients. Copyright 2006 S. Karger AG, Basel