In contrast, fenofibrate slightly increased ALAT (22 IU/L, P = 0.043). For 5 out of the 20 subjects values were above the normal range (Laboratory of Clinical Chemistry, University Hospital Maastricht, Maastricht, the Netherlands). Fenofibrate also increased ASAT (13 IU/L, P = 0.016L) and decreased ALP concentrations compared to placebo (−8 IU/L, P = 0.019). Creatinine concentrations were selleck products higher after fenofibrate treatment compared to placebo (9.8 μmol/L, P < 0.001) and fish oil treatment (9.4 μmol/L, P < 0.001). Although γ-GT did not change significantly (P = 0.979),

it slightly exceeded the normal range upon fenofibrate treatment compared to placebo for 4 out of 20 subjects. Overweight and obese subjects are often characterized by a disturbed lipid and lipoprotein profile, low-grade

systemic inflammation, and endothelial dysfunction. A way to improve these metabolic aberrations is by targeting PPARα. We hypothesized that a dietary intervention with n-3 LCPUFAs, as non-selective PPARα agonists, could be an alternative for a strong medicinal agonist. Therefore, we directly compared the effects of these n-3 LCPUFAs with those of fenofibrate on a broad range of biomarkers for cardiovascular disease. However, we found that fenofibrate (200 mg/d) and n-3 LCPUFA (3.7 g/d) treatment for 6 weeks did not improve markers for low-grade systemic inflammation and that fenofibrate had more profound effects on plasma see more lipids and vascular activity compared to fish oil in overweight and obese individuals. Studies on fenofibrate have shown inconsistent results regarding effects on low-grade inflammation and vascular activity [10], [11] and [12]. We found that fenofibrate reduced sE-selectin concentration compared to placebo and fish oil treatment in overweight and Gemcitabine order obese subjects. This finding corresponds to that of Hogue et al., who found in type 2 diabetic patients, that micronized fenofibrate

(200 mg/d) for 6 weeks reduced plasma sE-selectin, but did not affect concentrations of hsCRP, sICAM1 and sVCAM1 [11]. In contrast, Ryan et al. showed in an obese population, that fenofibrate reduced sVCAM1, sICAM1, TNFα, IL6, IL1β, but did not affect sE-selectin concentrations [12]. The reduced sE-selectin concentration as we observed suggests beneficial effects of fenofibrate on vascular activity, since E-selectin is involved in the adherence of leukocytes in the process of atherosclerosis [13]. However, this seems to contradict the observed increase in MCP1 concentrations after fenofibrate treatment compared to placebo, since this chemokine is responsible for attracting monocytes to the injured endothelium [13]. For fish oil, human intervention studies using doses ranging between 1.1 and 6.6 g/d n-3 LCPUFAs are inconsistent and do not often report beneficial effects on inflammatory markers and cellular adhesion molecules [14], [15], [16], [17] and [18].