title: Therapeutic effects of fibrates in postprandial lipemia.
abstract: Hypertriglyceridemia is observed in many metabolic diseases such as the metabolic syndrome, diabetes mellitus, or mixed dyslipidemia frequently leading to premature coronary heart disease (CHD). Additionally, several studies have shown that postprandial hypertriglyceridemia is pronounced in patients with CHD, metabolic syndrome, hypertension, and other pathologic conditions. The triglyceride-rich lipoprotein remnants accumulating in the postprandial state seem to be involved in atherogenesis and in events leading to thrombosis. Since abnormal postprandial lipemia is associated with pathologic conditions, its treatment is of clinical importance.Fibrates are of significant help in managing hypertriglyceridemia. This review summarizes the effect of fibric acid derivatives on postprandial lipemia. Fibrates decrease the production of and enhance the catabolism of triglyceride-rich lipoproteins through the activation of peroxisome proliferator-activated receptor-alpha. Results of clinical studies with fibrates have confirmed their action in decreasing postprandial triglyceride levels by increasing lipoprotein lipase activity, decreasing apolipoprotein CIII production, and by increasing fatty acid oxidation in the liver.It is concluded that fibrates are effective agents in lowering the postprandial increase in remnant lipoprotein particles and retinyl palmitate. Furthermore, fibrates can also affect the postprandial lipid profile by increasing hepatic lipase levels and in some cases, by reducing cholesterol ester transfer protein activity. The main target of fibrate therapy is to improve fasting hypertriglyceridemia, which is an essential component associated with improving postprandial lipemia. Fibrates are well tolerated by patients and adverse effects have been reported rarely after their administration.
authors.affiliation: 1st Cardiology Department, Onassis Cardiac Surgery Center, Athens, Greece. genovefa@kolovou.com
authors.forename: Genovefa D
authors.initials: GD
authors.lastname: Kolovou
authors.forename: Peggy M
authors.initials: PM
authors.lastname: Kostakou
authors.forename: Katherine K
authors.initials: KK
authors.lastname: Anagnostopoulou
authors.forename: Dennis V
authors.initials: DV
authors.lastname: Cokkinos
mesh_terms: D000818:Animals; D002986:Clinical Trials as Topic; D002995:Clofibric Acid / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy*; D000960:Hypolipidemic Agents / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D019518:Postprandial Period; D014280:Triglycerides / Q000097:blood
chemical_list: D000960:Hypolipidemic Agents; D014280:Triglycerides; D002995:Clofibric Acid