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.

Relationship Between Adiponectin and Left Atrium Size in Uncomplicated Obese Patients: Adiponectin, a Link Between Fat and Heart

“…On the contrary, the correlations between adiponectin vs. fasting blood glucose, insulin, triglycerides, HDL cholesterol concentrations, and HOMA-IR have been previously reported [36,37,[39][40][41][42][43]. The loss of significance after HOMA adjustment has also been indirectly assessed [44,45].…”

“…One likely explanation for this unusual similarity between lipid profiles could be the fasting state itself. The triglyceride-rich lipoprotein remnants accumulating in the postprandial state seem to be involved in atherogenesis and in events leading to thrombosis [40]. Moreover, the postprandial state causes an important increase in oxidative stress, especially in severely obese persons with greater insulin resistance [41].…”

Postprandial dysmetabolism: Too early or too late?

“…They are effective in lowering both fasting and postprandial triglycerides and triglyceride-rich lipoprotein (TRL) remnant particles. 154,165 It has also been suggested that fenofibrate may reduce fasting and postprandial inflammatory response and oxidative stress as it has been shown to reduce inflammation markers such as soluble vascular cell adhesion molecule-1 (VCAM-1) and soluble intercellular adhesion molecule-1 (ICAM-1) as well as oxidized fatty acids.…”

Postprandial lipemia as a cardiometabolic risk factor

“…Several studies have proven the efficacy of fibrates in reducing postprandial lipemia by increasing LPL activity, decreasing apoC-III production and increasing hepatic fatty acid oxidation as well as by decreasing secretion of VLDL particles, resulting in a significant reduction of TG levels (up to 50%) 145 . The GOLDN study showed that fibrate response in both the fasting and postprandial phase is affected by apoE polymorphisms, with E2 carriers exhibiting an increased postprandial response 146 .…”