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The combination of ezetimibe plus fenofibrate appeared to produce nearly identical alterations in serum lipoprotein levels when compared to monotherapy with 10 mg of atorvastatin. Daily treatment with the combination of ezetimibe plus fenofibrate is an acceptable alternative to atorvastatin for the treatment of dyslipidemia in patients who are intolerant of statins.
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Patients treated with peroxisome proliferator-activated receptor analogs (PPAR) alpha or alpha/gamma may develop a transient and reversible increase in serum creatinine, the mechanism of which remains obscure. This study evaluates whether treatment with either PPAR-alpha or -alpha/gamma analogs, fenofibrate or tesaglitazar, may cause deterioration in renal hemodynamics or exert direct tubular or glomerular nephrotoxic effects in rats.
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Peroxisome proliferator-activated receptor alpha (PPARalpha) activation in rodents is thought to improve insulin sensitivity by decreasing ectopic lipids in non-adipose tissues. Fenofibrate, a lipid-modifying agent that acts as a PPARalpha agonist, may prevent adipocyte hypertrophy and insulin resistance by increasing intracellular lipolysis from adipose tissue. Consistent with this hypothesis, fenofibrate decreased visceral fat mass and adipocyte size in high fat diet-fed obese mice, and concomitantly increased the expression of PPARalpha target genes involved in fatty acid beta-oxidation in both epididymal adipose tissue and differentiated 3T3-L1 adipocytes. However, mRNA levels of adipose marker genes, such as leptin and TNFalpha, were decreased in epididymal adipose tissue by fenofibrate treatment. Fenofibrate not only reduced circulating levels of free fatty acids and triglycerides, but also normalized hyperinsulinemia and hyperglycemia in obese mice. Blood glucose levels of fenofibrate-treated mice were significantly reduced during intraperitoneal glucose tolerance test compared with obese controls. These results suggest that fenofibrate-induced fatty acid beta-oxidation in visceral adipose tissue may be one of the major factors leading to decreased adipocyte size and improved insulin sensitivity.
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The daily water intake of 40 sexually mature male rats (groups II to V) was supplemented for 12 weeks with 10% fructose solution to induce hypertriglyceridemia. In addition, animals from three groups (III, IV, and V) were given through daily oral gavage metformin (group III), fenofibrate (group IV), and fish oil (group V) to estimate their therapeutic effects on fructose-induced metabolic alterations. Another group (I) of 10 rats served as controls. At 12 weeks, changes in sexual behavior and cavernous pressure response to nerve stimulation were correlated with serum triglyceride levels and response to preventive measures.
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In humans, fibrates are frequently used normolipidemic drugs. Fibrates act by regulating genes involved in lipoprotein metabolism via activation of the peroxisome proliferator-activated receptor-alpha (PPARalpha) in liver. In rodents, however, fibrates induce a peroxisome proliferation, leading to hepatomegaly and possibly hepatocarcinogenesis. Although this peroxisome proliferative response appears not to occur in humans, it remains controversial whether the beneficial effects of fibrates on lipoprotein metabolism can occur dissociated from such undesirable peroxisomal response. Here, we assessed the influence of fenofibrate on lipoprotein metabolism and peroxisome proliferation in the rabbit, an animal that, contrary to rodents and similar to humans, is less sensitive to peroxisome proliferators.
Male obese, IR and dyslipidemic E3L.CETP mice were treated with antidiabetic drugs rosiglitazone, liraglutide or an experimental 11β-hydroxysteroid-dehydrogenase-1 (HSD-1) inhibitor, or with hypolipidemic drugs atorvastatin, fenofibrate or niacin for 4-6 weeks. The effects on bw, IR and plasma and liver lipids were assessed.
AdipoR1 and AdipoR2 proteins were similarly abundant in preadipocytes and mature adipocytes despite an induction of mRNA expression during differentiation. Differentiation of 3T3-L1 cells in the presence of palmitic acid did not alter adiponectin receptor proteins but metformin and fenofibrate upregulated AdipoR2 within 24 h of incubation. AdipoR2 protein was significantly lower in human visceral compared to subcutaneous fat, and both receptors were reduced in visceral adipocytes. In rat tissues both receptors were reduced in visceral fat. In diabetic animals AdipoR2 protein, but not mRNA, was lower in both fat depots compared to similarly obese rats with normal glucose disposal. AdipoR1 was only reduced in subcutaneous adipose tissue of diabetic animals where mRNA expression was induced.
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The m204T>G variant was significantly associated with TG and HDL-C responses with fenofibrate. Individuals homozygous for the common T allele of m204T>G single nuclear polymorphism displayed both the greater reduction of TG (-32% for TT, -28% for GT, -25% for GG, P = 0.004) and an increase of HDL-C response compared with noncarriers (4.1% for TT, 3.4% for GT, 1.2% for GG, P = 0.01). Conversely, individuals homozygous for the minor allele of i6782C>T showed a greater increase in the HDL-C response compared with noncarriers (2.8% CC, 4.5% for CT, 5.8% for TT, P = 0.02), albeit no significant effect on TG response.
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Chronic toxicity studies of fenofibrate were carried out in rats (3 months), dogs (7 et 24 months) and Rhesus monkeys (12 months). The results in the last named species (78 animals) were of particular interest, since the treated monkeys had normal size liver without histological abnormalities. Electron microscopy showed no increase in the number of hepatic peroxisomes. Long-term toxicity studies in rats failed to show any increase in the incidence of altered hepatocytes or of neoplastic tumours in treated animals. However, a few peroxisomes were found in animals receiving the highest doses of fenofibrate. In reproduction studies there was no evidence of teratogenic effects in rats with doses 45 times higher than the human dose, nor in rabbits with doses of 300 mg/kg/day. In mutagenicity studies fenofibrate proved unable to bind with DNA and could not, therefore, have any effect on genes. The side-effects encountered in clinical practice (e.g. digestive disorders, sexual fatigue, myalgia, alopecia) were rare and obliged to discontinue treatment in very few cases. Long-term clinical trials failed to demonstrate any fenofibrate-induced pathology, such as malignant or benign tumours, or biliary or urinary lithiasis. Serum transaminases were increased in 10 to 20% of the patients, but the rise was transient and never reached pathological levels. Electron microscope study of liver biopsies from patients treated with fenofibrate showed no proliferation of peroxisomes.
EtFSC, but not AqFSC, significantly elevated hepatic triglyceride (TG) in mice fed with ND. Feeding mice with HFCBD increased serum total cholesterol (TC), high density lipoprotein (HDL) and low density lipoprotein (LDL) levels as well as alanine aminotransferase (ALT) activity. Supplementation with AqFSC, EtFSC or fenofibrate significantly reduced hepatic TC and TG levels. However, AqFSC and EtFSC supplementation increased serum HDL and LDL levels in mice fed with HFCBD. Fenofibrate increased serum HDL and reduced serum LDL contents in hypercholesterolemic mice. EtFSC reduced, but fenofibrate elevated, serum ALT activity in both normal and hypercholesterolemic mice. While fenofibrate reduced serum TC, TG, and HDL levels in mice fed with ND, it increased serum HDL and reduced serum LDL and TC levels in mice fed with HFCBD. Hepatomegaly was found in normal and hypercholesterolemic mice fed with diet supplemented with fenofibrate.