Abstract 11454: Bezafibrate Improves Postprandial Hypertriglyceridemia and Postprandial Endothelial Dysfunction in Patients With Metabolic Syndrome by decreasing Endogenous Triglyceride Level Rather Than Reducing Absorption After Meal Test
Background: Postprandial elevation of triglyceride (TG) has been shown to impair endothelial function and considered as residual risks. We investigated the postprandial effects of bezafibrate on endothelial dysfunction and lipid profile.
Methods: A randomized cross-over trial design in 10 patients with metabolic syndrome (43±10 years, BMI 28.4±3.9 kg/m2) was performed. Lipid profiles including CM-TG, VLDL-TG and LDL-TG, ApoB48, glucose and endothelial function assessed by brachial artery flow-mediated dilation (FMD) during a fasting state and at 2, 4, 6 and 8 h after a standard meal loading test fat 30 kcal/m2) were determined before and after bezafibrate treatment (200mg/day) for one month.
Results: Bezafibrate treatment significantly suppressed postprandial elevation in serum level of TG (incremental area under the curve [iAUC]; from 1211 ± 344 to 536 ± 76 mgh/dl, p=0.03), ApoB-48 (iAUC; form 49.0 ± 12.4 to 26.1 ± 3.8μgh/ml, p=0.02) and remnant like particles cholesterol (RLP-C) (iAUC; form 68 ± 18 to 27 ± 4 mgh/ml, p=0.03). Glucose metabolism did not change after bezafibrate treatment. Postprandial endothelial dysfunction assessed by FMD was significantly improved after bezafibrate treatment (maximum percent decrease in FMD, from -41.4 ±6.6 % to -26.1±4.5%, p=0.04). At 4h after meal loading test, bezafibrate treatment significantly reduced CM-TG, VLDL-TG and LDL-TG respectively, while the decrease in postprandial TG is mainly due to the decrease in VLDL-TG and LDL-TG rather than CM-TG. The decrease in nominal FMD was significantly associated with the maximum change in triglyceride(r=-0.49, p=0.04) . Change in glucose level was not associated with the maximum change in FMD.
Conclusion: Bezafibrate significantly improved postprandial hypertriglyceridemia and endothelial dysfunction in patients with metabolic syndrome mainly due to improvement of endogenous TG metabolism.
- © 2013 by American Heart Association, Inc.