Disease relevance of Etofibrate

• We evaluated the effect of etofibrate on the LDL-subtype distribution in patients with type 2 diabetes mellitus (n = 13, 55 +/- 18 years, BMI 27.9 +/- 5.5 kg/m2, HbA1c 10.1 +/- 3.9 %) and diabetic dyslipoproteinemia (triglycerides 343 +/- 253 mg/dl, HDL-cholesterol 36 +/- 7 mg/dl, LDL-cholesterol 110 +/- 37 mg/dl) [1].
• Effect of etofibrate on the development and the regression of atheromas in a rabbit model of atherosclerosis [2].
• One of the groups received daily 200 mg Etofibrate/kg body weight, the other not [2].
• Ten patients with myocardial infarction and 10 arteriosclerosis obliterans patients were treated with Etofibrate (900 mg/day) for 12 weeks [3].
• On the basis of our observations Etofibrate may be useful in the therapy of arteriosclerotic vascular diseases with or without hyperlipaemia, because it could decrease the cellular sensitization against aortic tissue [3].

High impact information on Etofibrate

• Therefore, a potent effect of etofibrate on both chylomicron lipolysis and remnant removal was achieved, indicating that this drug can be used to improve this metabolism in future prospective studies [4].
• Effects of etofibrate upon the metabolism of chylomicron-like emulsions in patients with coronary artery disease [4].
• These findings in patients with HPL Type II indicate in vivo upregulation of specific [111In]LDL as well as [111In]HDL binding sites on human platelets associated with reduced platelet activation following etofibrate therapy [5].
• Following a 6-week treatment period with etofibrate (500 mg twice daily), decrease in plasma total cholesterol, LDL-cholesterol and apolipoprotein (apo) B and increase in HDL-cholesterol and apo AI was correlated to a significant (P < 0.01) increase in LDL- as well as HDL-receptor binding [5].
• Influence of Etofibrate on plasma fibrinogen and plasminogen concentrations in patients with different forms of primary hyperlipoproteinemia [6].

Chemical compound and disease context of Etofibrate

• Addition of 200 mg Etofibrate/kg body weight per day to the cholesterol-enriched food caused a significant inhibition of the proliferation of the smooth muscle cells in the intimal proliferate which consequently resulted in a less pronounced plaque [2].
• The study presents the effect of 2-[2-(p-Chlorophenoxy)-2-methylproprionoxy]ethyl nicotinate (Etofibrate, Lipo-Merz) on progression and regression of experimentally induced atheromas [2].
• To understand the mechanism by which the drug affects plasma triacylglycerols, normolipemic rats were treated daily with 300 mg of etofibrate/kg body weight or with the medium by a stomach tube [7].

Biological context of Etofibrate

• In conclusion, injury-induced neointima formation is reduced in etofibrate-treated animals, which could be due to an inhibition of smooth muscle cell proliferation [8].
• Plasmolysis, red blood cell partitioning, and plasma protein binding of etofibrate, clofibrate, and their degradation products [9].
• Nicotinic acid produced a slight enhancement of antibody responses to sheep erythrocytes, whereas etofibrate inhibited the response at the highest dose studied [10].
• High performance liquid chromatographic determination of etofibrate and its hydrolysis products [11].
• Etofibrate treatment alters low density lipoprotein susceptibility to lipid peroxidation [12].

Anatomical context of Etofibrate

• Etofibrate suppresses neointima formation of the ballooned common carotid artery of rats [8].
• Studies with etofibrate in the rat. Part II: A comparison of the effects of prolonged and acute administration on plasma lipids, liver enzymes and adipose tissue lipolysis [13].
• In animals on prolonged treatment etofibrate decreased plasma levels of cholesterol, triacylglycerols, free fatty acids (FFA) and glycerol, as well as the total and unesterified cholesterol concentrations, in liver microsomes [13].

Associations of Etofibrate with other chemical compounds

• In addition, triglyceride-lowering treatment with etofibrate only slightly improves markers of fasting and postprandial hemostasis in an antithrombotic and profibrinolytic direction [14].
• In a controlled clinical trial with a placebo prephase, the comparison of the two lipid-lowering drugs etofibrate and gemfibrozil showed no clinically relevant differences of lipoprotein profile modification in 50 patients with combined hyperlipidaemia [15].
• Epididymal fat pad pieces from etofibrate-treated rats incubated in vitro released more glycerol but the same amount of FFA to the medium, and had greater uptake of [U-14C]glycerol for [14C]acylglycerol formation [7].
• The clofibric acid levels in blood are studied after the oral administration of 500 mg of etofibrate given as a unique dose in three different delayed-release tablets [16].
• However, with the exception of a significant reduction in cytosolic glycerol-3-P dehydrogenase at 7 h and in ACAT at 5 h, acute etofibrate treatment did not affect the activity of the liver enzymes studied [13].

Gene context of Etofibrate

• HMG-CoA reductase and acylCoA cholesterol acyltransferase were decreased while cholesterol 7 alpha-hydroxylase was not significantly modified by etofibrate [17].
• The hypocholesterolemic effect of etofibrate after acute treatment may be a secondary consequence of the reduced liver VLDL production caused by decreased adipose tissue lipolysis, but after prolonged treatment, this effect also seems to be influenced by the inhibition of HMG-CoA reductase activity which would reduce cholesterol synthesis [13].
• In dyslipidemic or hyperlipidemic patients etofibrate (CAS 31637-97-5, active principle of Lipo-Merz-retard) improves plasma lipoprotein profiles by reducing low density lipoprotein cholesterol and triglycerides [18].

Analytical, diagnostic and therapeutic context of Etofibrate

• Plasma lipids (enzymatic methods) and LDL-subtypes (7 LDL-subfractions, density gradient ultracentrifugation) were measured before and during etofibrate therapy (500 mg/d, 7 - 16 weeks) [1].
• To answer these questions, we measured markers of hemostasis immediately before a standardized fatty meal, and 4, 6, 8, and 10 hours after the meal in 21 hypertriglyceridemic men both before and after treatment with etofibrate [14].
• High performance liquid chromatographic (HPLC) method is presented for the determination of etofibrate (EF) and its hydrolysis products [11].
• We investigated the changes in serum lipid concentrations of patients treated with Etofibrate as part of their routine management in the metabolic ambulatory care unit of the Medical Policlinic at the University of Marburg [19].
• In the patients treated with etofibrate, the range of the lithogenic index remained stable with 0.89-1.69 before and 0.78-1.51 after 5 day drug therapy [20].

References