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Fenofibrate-loaded LFCS Type III SNEDDS formulations could be a potential oral pharmaceutical product for administering the poorly water-soluble drug, fenofibrate, with an enhanced oral BA.
tricor cholesterol medicine
Alterations in Abcb4(-/-) mice, compared with wild-type mice, included deregulation of genes that control lipid synthesis, storage, and oxidation; decreased serum levels of cholesterol and phospholipids; and reduced hepatic long-chain fatty acyl-CoAs (LCA-CoA). Feeding Abcb4(-/-) mice the side chain-modified bile acid 24-norursodeoxycholic acid (norUDCA) reversed their liver injury and fibrosis, increased serum levels of lipids, lowered phospholipase and triglyceride hydrolase activities, and restored hepatic LCA-CoA and triglyceride levels. Additional genetic and nutritional studies indicated that lipid metabolism contributed to chronic cholestatic liver injury; crossing peroxisome proliferator-activated receptor (PPAR)-α-deficient mice with Abcb4(-/-) mice (to create double knockouts) or placing Abcb4(-/-) mice on a high-fat diet protected against liver injury, with features similar to those involved in the response to norUDCA. Placing pregnant Abcb4(-/-) mice on high-fat diets prevented liver injury in their offspring. However, fenofibrate, an activator of PPARα, aggravated liver injury in Abcb4(-/-) mice.
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Fenofibrate was associated with a 19% reduction in serum urate after 3 weeks of treatment (mean+/-S.E. 0.37+/-0.04 vs 0.30+/-0.02 mM/l; P=0.004). The effect was reversed after a 3-week fenofibrate withdrawal period (0.30+/-0.02 vs 0.38+/-0.03 mM/l). There was a rise in uric acid clearance with fenofibrate treatment of 36% (7.2+/-0.9 vs 11.4+/-1.6 ml/min, normal range 6-11; P=0.006) without a significant change in creatinine clearance. Both total cholesterol and serum triglycerides were also reduced. No patient developed acute gout whilst taking fenofibrate.
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In the primary prevention of atherosclerosis and risk of lipoproteinemia, is of primordial importance. Therefore, adequate food and physical activities are necessary. If no good result is evident thereafter medicinal treatment should be prescribed. In our open random study performed in two different centres, we evaluated the efficiency and tolerance of Gemfibrozile and Phenofibrate in 77 patients with IIa, IIb, and IV stage of hyperlipoproteinaemia. The study included the patients in whom the 8-week diet gave no expected results. The evaluation of Gemfibrosile (900 mg daily) and Phenofibrate (300 m daily) efficiency lasted 12 weeks. During that time 11 patients were excluded from the study because of administration of other relevant drugs or for lack of control examinations. The efficiency was evaluated in 66 patients: 33 to Gemfibrozile and 31 to Phenofibrate. At the end of treatment the following results were obtained: decreased cholesterol level by 17% in Gemfibrozile patients and by 6% in Phenofibrate subjects; LDL-cholesterol by 15% i.e. 3% and triglycerides by 48% in Gemfibrozile cases and by 27% in Phenofibrate individuals. At the end of treatment HDL-cholesterol was increased by 29% in patients treated with Gemfibrozile and by 9% in those treated with Phenofibrate. Apoprotein A-1 was increased after Phenofibrate treatment and decreased after Gemfibrozile administration. Apoprotein B was increased in both groups. No harmful clinical or laboratory effects were observed. On the basis of these results it can be concluded that the effect of Gemfibrozile was more favourable on lipod composition in the plasma then that of Phenofibrate. No significant differences in drug tolerance were observed.
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We observed statistically significant increases in concentrations of serum creatinine (P < 0.005) and cystatin C(P < 0.01). Concentrations of both analytes increased in 10 (83.3%) of the patients. In these patients, the median increases were 15.1% (range 5.5-23.2%) for creatinine and 9.9% (range 1.1-26.1%) for cystatin C.
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The blood-brain barrier contributes to maintain brain cholesterol metabolism and protects this uniquely balanced system from exchange with plasma lipoprotein cholesterol. Brain capillary endothelial cells, representing a physiological barrier to the central nervous system, express apolipoprotein A-I (apoA-I, the major high-density lipoprotein (HDL)-associated apolipoprotein), ATP-binding cassette transporter A1 (ABCA1), and scavenger receptor, class B, type I (SR-BI), proteins that promote cellular cholesterol mobilization. Liver X receptors (LXRs) and peroxisome-proliferator activated receptors (PPARs) are regulators of cholesterol transport, and activation of LXRs and PPARs has potential therapeutic implications for lipid-related neurodegenerative diseases. To clarify the functional impact of LXR/PPAR activation, sterol transport along the: (i) ABCA1/apoA-I and (ii) SR-BI/HDL pathway was investigated in primary, polarized brain capillary endothelial cells, an in vitro model of the blood-brain barrier. Activation of LXR (24(S)OH-cholesterol, TO901317), PPARalpha (bezafibrate, fenofibrate), and PPARgamma (troglitazone, pioglitazone) modulated expression of apoA-I, ABCA1, and SR-BI on mRNA and/or protein levels without compromising transendothelial electrical resistance or tight junction protein expression. LXR-agonists and troglitazone enhanced basolateral-to-apical cholesterol mobilization in the absence of exogenous sterol acceptors. Along with the induction of cell surface-located ABCA1, several agonists enhanced cholesterol mobilization in the presence of exogenous apoA-I, while efflux of 24(S)OH-cholesterol (the major brain cholesterol metabolite) in the presence of exogenous HDL remained unaffected. Summarizing, in cerebrovascular endothelial cells apoA-I, ABCA1, and SR-BI represent drug targets for LXR and PPAR-agonists to interfere with cholesterol homeostasis at the periphery of the central nervous system.
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To assess the efficacy and safety of K-877 (Pemafibrate), a novel selective peroxisome proliferator-activated receptor α modulator (SPPARMα) that possesses unique PPARα activity and selectivity, compared with placebo and fenofibrate in dyslipidaemic patients with high triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-C) levels.
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The effect of fenofibrate, a ligand of peroxisome proliferator-activated receptor (PPAR) alpha, on the growth and metastatic potential of Bomirski hamster melanoma s.c. tumors, pigmented line (BHM Ma) was investigated in vivo. RT-PCR and Western-blot analyses revealed the presence of mRNA and protein of PPAR alpha in BHM Ma cells. The animals treated orally with fenofibrate developed significantly fewer metastatic foci in the lungs, as compared to the control group; however, primary tumor growth remained unaltered. This observation is interesting in respect of the potential use of fenofibrate in melanoma chemoprevention.
We show that PPARalpha protein, like primary human monocytes, is also expressed in the human monocytic THP-1 cell line. Fenofibric acid, WY14643, and GW2331 inhibited TF mRNA upregulation after stimulation of THP-1 cells with lipopolysaccharide or interleukin-1ss. In primary human monocytes and macrophages, the lipopolysaccharide- or interleukin-1ss-mediated induction of TF activity was also inhibited by fenofibric acid, WY14643, or GW2331.
The effects on serum lipoproteins were studied in 8 patients with familial heterozygous hypercholesterolemia and 9 patients with familial combined hyperlipidemia during an 8-week treatment with fenofibrate. VLDL, IDL, LDL and HDL were isolated by ultracentrifugation and precipitation. Lipids and apolipoproteins A-I and B were determined by enzymatic and immunonephelometric techniques, respectively. In hypercholesterolemia, administration of fenofibrate resulted in decreases of VLDL, IDL, and LDL (cholesterol -58.3%, -28.6%, and -24.4%), while, in combined hyperlipidemia, treatment with the drug lowered VLDL and IDL (-33.3% and -42.9%). HDL cholesterol and apolipoprotein A-I increased only in hypercholesterolemia (+22.9% and +6.9%).