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Effects of fenofibrate on endothelial function and cell adhesion molecules during post‐prandial lipemia in hypertriglyceridemia
Author(s) -
Marchesi S.,
Lupattelli G.,
Lombardini R.,
Roscini A. R.,
Siepi D.,
Vaudo G.,
Pirro M.,
Sinzinger H.,
Schillaci G.,
Mannarino E.
Publication year - 2003
Publication title -
journal of clinical pharmacy and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.622
H-Index - 73
eISSN - 1365-2710
pISSN - 0269-4727
DOI - 10.1046/j.0269-4727.2003.00512.x
Subject(s) - fenofibrate , hypertriglyceridemia , medicine , endocrinology , vasodilation , chemistry , postprandial , endothelial dysfunction , triglyceride , endothelium , cholesterol , diabetes mellitus
Summary Background: Fasting and post‐prandial hypertriglyceridemia have been associated with endothelial dysfunction. Objective: To investigate the effects of a 3‐month treatment with fenofibrate (200 mg daily) on endothelial reactivity and inflammatory state in hypertriglyceridemic patients at fast and after an oral fat load. Methods: Brachial flow‐mediated vasodilation (FMV) and the circulating levels of intercellular adhesion molecule (ICAM) and vascular cellular adhesion molecule (VCAM) were determined in 10 hypertriglyceridemic patients. Results: Before treatment, post‐prandial phase was characterized by an increase in triglycerides (3·7 ± 1 mmol/L at baseline vs. 4·2 ± 1, 6·5 ± 1, 6·6 ± 2, and 5·3 ± 2 mmol/L after 2, 4, 6, and 8 h), a decrease in FMV (4·3 ± 2% at baseline vs. 2·8 ± 1, 2·2 ± 1, and 1·3 ± 1% after 2, 4, and 6 h), and an increase in ICAM and VCAM. After fenofibrate there was a significant reduction in fasting triglycerides (3·7 ± 1·3 vs. 2·1 ± 0·8 mmol/L), ICAM (480 ± 113 vs. 269 ± 65 ng/mL) and VCAM (1821 ± 570 vs. 1104 ± 376 ng/mL), and an increase in FMV (4·3 ± 2 vs. 7·1 ± 2%). Post‐prandially triglycerides increased (2·1 ± 1 at baseline vs. 2·4 ± 2 and 3·6 ± 1 mmol/L after 4 and 6 h), FMV decreased (7·1 ± 2 at baseline vs. 5·8 ± 2, 5·5 ± 2, 5·9 ± 2, 6·4 ± 2% after 2, 4, 6, and 8 h), and there was an increase of ICAM and VCAM. Before therapy post‐prandial changes in FMV had an inverse correlation with the changes in triglycerides ( r = −0·34; P < 0·05) and ICAM ( r = −0·66; P < 0·001). Conclusions: The transient endothelial dysfunction observed in hypertriglyceridemic subjects during post‐prandial lipemia is mediated by post‐prandial triglyceride increase and by the activation of inflammatory response. The anti‐inflammatory activity of fenofibrate may represent an additional mechanism of its favorable action on the endothelial function during fasting and the post‐prandial phase.