An antilipemic agent that lowers CHOLESTEROL and TRIGLYCERIDES. It decreases LOW DENSITY LIPOPROTEINS and increases HIGH DENSITY LIPOPROTEINS.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
TRANSCRIPTION FACTORS that are activated by ligands and heterodimerize with RETINOID X RECEPTORS and bind to peroxisome proliferator response elements in the promoter regions of target genes.
An antilipemic agent that is the biologically active metabolite of CLOFIBRATE.
Compounds that either share the structure of fibric acid in their molecular arrangement or are considered variants of the fibric acid structure.
A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol.
An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.
A condition of elevated levels of TRIGLYCERIDES in the blood.
A flavoprotein oxidoreductase that has specificity for long-chain fatty acids. It forms a complex with ELECTRON-TRANSFERRING FLAVOPROTEINS and conveys reducing equivalents to UBIQUINONE.
A fibric acid derivative used in the treatment of HYPERLIPOPROTEINEMIA TYPE III and severe HYPERTRIGLYCERIDEMIA. (From Martindale, The Extra Pharmacopoeia, 30th ed, p986)
Enlargement of the liver.
Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.
A nuclear transcription factor. Heterodimerization with RETINOID X RECEPTOR GAMMA is important to metabolism of LIPIDS. It is the target of FIBRATES to control HYPERLIPIDEMIAS.

Heterotropic effectors exert more significant strain on monoligated than on unligated hemoglobin. (1/221)

The effect of allosteric effectors, such as inositol hexakisphosphate and/or bezafibrate, has been investigated on the unliganded human adult hemoglobin both spectroscopically (employing electronic absorption, circular dichroism, resonance Raman, and x-ray absorption near-edge spectroscopies) and functionally (following the kinetics of the first CO binding step up to a final 4% ligand saturation degree). All data indicate that the unliganded T-state is not perturbed by the interaction with either one or both effectors, suggesting that their functional influence is only exerted when a ligand molecule is bound to the heme. This is confirmed by the observation that CO dissociation from partially liganded hemoglobin ( +info)

Variation of liver-type fatty acid binding protein content in the human hepatoma cell line HepG2 by peroxisome proliferators and antisense RNA affects the rate of fatty acid uptake. (2/221)

The liver-type fatty acid binding protein (L-FABP), a member of a family of mostly cytosolic 14-15 kDa proteins known to bind fatty acids in vitro and in vivo, is discussed to play a role in fatty acid uptake. Cells of the hepatoma HepG2 cell line endogenously express this protein to approximately 0.2% of cytosolic proteins and served as a model to study the effect of L-FABP on fatty acid uptake, by manipulating L-FABP expression in two approaches. First, L-FABP content was more than doubled upon treating the cells with the potent peroxisome proliferators bezafibrate and Wy14,643 and incubation of these cells with [1-14C]oleic acid led to an increase in fatty acid uptake rate from 0.55 to 0.74 and 0.98 nmol/min per mg protein, respectively. In the second approach L-FABP expression was reduced by stable transfection with antisense L-FABP mRNA yielding seven clones with L-FABP contents ranging from 0.03% to 0.14% of cytosolic proteins. This reduction to one sixth of normal L-FABP content reduced the rate of [1-14C]oleic acid uptake from 0.55 to 0. 19 nmol/min per mg protein, i.e., by 66%. The analysis of peroxisome proliferator-treated cells and L-FABP mRNA antisense clones revealed a direct correlation between L-FABP content and fatty acid uptake.  (+info)

Coupling of the oxygen-linked interaction energy for inositol hexakisphosphate and bezafibrate binding to human HbA0. (3/221)

The energetics of signal propagation between different functional domains (i.e. the binding sites for O2, inositol hexakisphospate (IHP), and bezafibrate (BZF)) of human HbA0 was analyzed at different heme ligation states and through the use of a stable, partially heme ligated intermediate. Present data allow three main conclusions to be drawn, and namely: (i) IHP and BZF enhance each others binding as the oxygenation proceeds, the coupling free energy going from close to zero in the deoxy state to -3.4 kJ/mol in the oxygenated form; (ii) the simultaneous presence of IHP and BZF stabilizes the hemoglobin T quaternary structure at very low O2 pressures, but as oxygenation proceeds it does not impair the transition toward the R structure, which indeed occurs also under these conditions; (iii) under room air pressure (i.e. pO2 = 150 torr), IHP and BZF together induce the formation of an asymmetric dioxygenated hemoglobin tetramer, whose features appear reminiscent of those suggested for transition state species (i.e. T- and R-like tertiary conformation(s) within a quaternary R-like structure).  (+info)

A comparison of the use, effectiveness and safety of bezafibrate, gemfibrozil and simvastatin in normal clinical practice using the New Zealand Intensive Medicines Monitoring Programme (IMMP). (4/221)

AIMS: Because of the importance of treating dyslipidaemia in the prevention of ischaemic heart disease and because patient selection criteria and outcomes in clinical trials do not necessarily reflect what happens in normal clinical practice, we compared outcomes from bezafibrate, gemfibrozil and simvastatin therapy under conditions of normal use. METHODS: A random sample of 200 patients was selected from the New Zealand Intensive Medicines Monitoring Programme's (IMMP) patient cohorts for each drug. Questionnaires sent to prescribers requested information on indications, risk factors for ischaemic heart disease, lipid profiles with changes during treatment and reasons for stopping therapy. RESULTS: 80% of prescribers replied and 83% of these contained useful information. The three groups were similar for age, sex and geographical region, but significantly more patients on bezafibrate had diabetes and/or hypertension than those on gemfibrozil or simvastatin. After treatment and taking the initial measure into account, the changes in serum lipid values were consistent with those generally observed, but with gemfibrozil being significantly less effective than expected. More patients (15.8%S) stopped gemfibrozil because of an inadequate response compared with bezafibrate (5.4%) and simvastatin (1.6%). Gemfibrozil treatment was also withdrawn significantly more frequently due to a possible adverse reaction compared with the other two drugs. CONCLUSIONS: In normal clinical practice in New Zealand gemfibrozil appears less effective and more frequently causes adverse effects leading to withdrawal of treatment than either bezafibrate or simvastatin.  (+info)

Phytanic acid is ligand and transcriptional activator of murine liver fatty acid binding protein. (5/221)

Branched-chain phytanic acid is metabolized in liver peroxisomes. Sterol carrier protein 2/sterol carrier protein x (SCP2/SCPx) knockout mice, which develop a phenotype with a deficiency in phytanic acid degradation, accumulate dramatically high concentrations of this fatty acid in serum (Seedorf at al. 1998. Genes Dev. 12: 1189-1201) and liver. Concomitantly, a 6.9-fold induction of liver fatty acid binding protein (L-FABP) expression is observed in comparison to wild-type animals fed standard chow, possibly mediated by the peroxisome proliferator-activated receptor alpha (PPARalpha). Cytosolic transport of phytanic acid to either peroxisomal membranes or to the nucleus for activation of PPARalpha may be mediated by L-FABP, which gives rise to the question whether phytanic acid is a transactivator of this protein. Here we show first that phytanic acid binds to recombinant L-FABP with high affinity. Then the increase of the in vivo phytanic acid concentration by phytol feeding to mice results in a 4-fold induction of L-FABP expression in liver, which is in the order of that attained with bezafibrate, a known peroxisome proliferator. Finally to test in vitro whether this induction is conferred by phytanic acid, we cotransfected HepG2 cells with an expression plasmid for murine PPARalpha and a CAT-reporter gene with 176 bp of the murine L-FABP promoter, containing the peroxisome proliferator responsive element (PPRE). After incubation with phytanic acid, we observed a 3.2-fold induction of CAT expression. These findings, both in vivo and in vitro, demonstrate that phytanic acid is a transcriptional activator of L-FABP expression and that this effect is mediated via PPARalpha.  (+info)

The effect of peroxisome proliferators on mitochondrial bioenergetics. (6/221)

Peroxisome proliferators are a group of structurally diverse chemicals that cause the proliferation of peroxisomes in rodents. The purpose of this investigation was to test the hypothesis that the shared effect of these compounds on peroxisome proliferation is mediated through a common inhibitory effect on mitochondrial bioenergetics. Freshly isolated rat liver mitochondria were energized with succinate. The effect of the chemicals on mitochondrial bioenergetics was analyzed by monitoring calcium-induced changes in membrane potential and swelling, as well as changes in mitochondrial respiration. Mitochondrial membrane potential was measured with a TPP(+)-sensitive electrode, and swelling was recorded spectrophotometrically. Mitochondrial oxygen uptake was monitored with a Clark-type oxygen electrode. Gemfibrozil and WY-14,643 induced the mitochondrial permeability transition as characterized by calcium-induced swelling and depolarization of membrane potential, both of which were inhibited by cyclosporine A. Fenofibrate, clofibrate, ciprofibrate and diethylhexyl phthalate, on the other hand, caused a direct dose-dependent depolarization of mitochondrial membrane potential. However, the mechanism of membrane depolarization varied among the test chemicals. Bezafibrate and trichloroethylene elicited no effect on succinate-supported mitochondrial bioenergetics. The results of this investigation demonstrate that although most, but not all, peroxisome proliferators interfere with mitochondrial bioenergetics, the specific biomolecular mechanism differs among the individual compounds.  (+info)

Activators of peroxisome proliferator-activated receptor-alpha induce the expression of the uncoupling protein-3 gene in skeletal muscle: a potential mechanism for the lipid intake-dependent activation of uncoupling protein-3 gene expression at birth. (7/221)

The recently identified uncoupling protein-3 (UCP-3) gene, predicted to encode a new member of the family of uncoupling proteins, is preferentially expressed in skeletal muscle and has been related to phenotypes of obesity and type 2 diabetes. We have established that during mouse ontogeny, the expression of the UCP-3 gene is switched on in skeletal muscle just after birth. The induction of UCP-3 gene expression is dependent on the initiation of suckling and particularly on lipid intake. Treatment of newborn mice with activators of peroxisome proliferator-activated receptors (PPARs), such as clofibrate, bezafibrate, or (4-chloro-6-(2,3-xylidine)-pirimidinylthio)acetic acid (WY 14,643), mimics the action of food intake on UCP-3 gene expression. The specific ligand of PPAR-alpha WY 14,643 induces UCP-3 gene expression in a time- and dose-dependent manner, whereas the thiazolidinedione BRL 49653, specific for PPAR-gamma, has no effect. These treatments act without altering circulating free fatty acids. During development, skeletal muscle expresses constitutive levels of PPAR-delta mRNA, whereas expression of the PPAR-gamma gene is undetectable. PPAR-alpha gene expression is developmentally regulated in muscle as it is first expressed at birth, just before UCP-3 gene induction occurs. The induction of UCP-3 gene expression by WY 14,643 is impaired in skeletal muscle of premature neonates, which do not express PPAR-alpha. It is proposed that the UCP-3 gene is predominantly regulated in neonatal muscle by PPAR-alpha activation.  (+info)

Effects of fibrate compounds on expression of plasminogen activator inhibitor-1 by cultured endothelial cells. (8/221)

The consistent positive correlation between triglyceride and plasminogen activator inhibitor-1 (PAI-1) levels in plasma and the fact that very low density lipoprotein (VLDL) induces secretion of PAI-1 from cultured human umbilical vein endothelial cells (HUVECs) and human hepatoblastoma cells have raised the question of whether fibrate treatment, the main effect of which is a profound lowering of plasma concentrations of VLDL, might improve fibrinolytic function by reducing the plasma levels of PAI-1. However, the findings of controlled clinical trials using various fibrate compounds have been discrepant. ECs express PAI-1 under normal conditions in humans. We therefore examined the effects of several fibrate compounds on PAI-1 expression and secretion by cultured HUVECs and the HUVEC-derived cell line EA.hy926. All fibrate compounds examined had significant effects on PAI-1 gene transcription in the EA.hy926 cells. Low concentrations of clofibric acid and bezafibrate increased PAI-1 transcription and secretion, whereas Wy-14643 increased PAI-1 synthesis in a dose-dependent way. In contrast, both fenofibric acid and gemfibrozil markedly decreased PAI-1 transcription and secretion from HUVECs and EA.hy926 cells. Thus, stimulation of the transcriptional activity of the PAI-1 gene by some fibrates is linked to increased secretion of PAI-1 protein by the cells, whereas the opposite effects occur with other fibrate compounds. Whether the different effects on PAI-1 transcription and secretion by ECs in vitro also reflect differences in treatment effects on the regulation of plasma PAI-1 activity in vivo will have to be determined in larger-scale, controlled clinical trials.  (+info)

Recent data support the renewed interest in hypertriglyceridemia as a possible important therapeutic target for cardiovascular risk reduction. This study was designed to address the question of all-cause mortality during extended follow-up of the BIP trial in patients stratified by baseline triglyceride levels. In the BIP trial 3090 patients with proven coronary artery disease were randomized to bezafibrate 400 mg/day or placebo. All-cause mortality data after 20 years of follow-up, were obtained from the National Israeli Population Registry. Patients with hypertriglyceridemia (triglycerides ≥200 mg/dL, n = 458) were equally distributed among the study groups (15 % in both placebo and bezafibrate groups). During follow-up 1869 patients died (952 in placebo vs. 917 in bezafibrate group). Following multivariate adjustment allocation to bezafibrate was associated with small but significant 10 % mortality risk reduction (HR 0.90; 95 % CI 0.82-0.98, p = 0.026). Variables associated with significantly
Drug-induced gene expression patterns that invert disease profiles have recently been illustrated to be a new strategy for drug-repositioning. In the present study, we validated this approach and focused on prediction of novel drugs for lung adenocarcinoma (AC), for which there is a pressing need to find novel therapeutic compounds. Firstly, connectivity map (CMap) analysis computationally predicted bezafibrate as a putative compound against lung AC. Then this hypothesis was verified by in vitro assays of anti-proliferation and cell cycle arrest. In silico docking evidence indicated that bezafibrate could target cyclin dependent kinase 2(CDK2), which regulates progression through the cell cycle. Furthermore, we found that bezafibrate can significantly down-regulate the expression of CDK2 mRNA and p-CDK2. Using a nude mice xenograft model, we also found that bezafibrate could inhibit tumor growth of lung AC in vivo. In conclusion, this study proposed bezafibrate as a potential therapeutic option for lung
This study provides strong evidence that bezafibrate has antidiabetic properties, supporting both in vitro data and earlier post hoc analyses suggesting that bezafibrate can prevent or delay the onset of type 2 diabetes (5-7). It further indicates that this effect is unique to bezafibrate among the fibrates. These findings have important implications for research. Our findings are bolstered by the similarity of subjects in exposure groups on clinically relevant characteristics, the fact that the finding of a protective effect is of a clinically relevant magnitude, statistically significant, and robust to sensitivity analyses including adjustment for BMI, and the monotonic duration-response relationship.. The results of the post hoc analysis are reassuring. It was reasonable to worry that fenofibrate was more likely to be prescribed to individuals with a high risk for diabetes or unrecorded diabetes, creating a falsely elevated hazard for development of diabetes during fenofibrate treatment ...
PubMed journal article: Relation of clinical benefit of raising high-density lipoprotein cholesterol to serum levels of low-density lipoprotein cholesterol in patients with coronary heart disease (from the Bezafibrate Infarction Prevention Trial). Download Prime PubMed App to iPhone, iPad, or Android
In the search for new potential antihyperlipidemic agents, the present study focuses on the synthesis of novel N-(benzoylphenyl)-5-substituted-1H-indole-2-carboxamides (compounds 8-12, 15, 16, 18) and investigating their antihyperlipidemic activity using Triton WR-1339-induced hyperlipidemic rats as an experimental model. Hyperlipidemia was developed by intraperitoneal injection of Triton WR-1339 (250 mg/kg body weight). The tested animals were divided into normal control (NCG), hyperlipidemic (HG), compound 8, 9, 15, 16, 18- and bezafibrate treated groups. At a dose of 15 mg/kg body weight, compounds 9, 16, 18 and bezafibrate (100 mg/kg) significantly (p | 0.0001) reduced elevated plasma triglycerides levels after 12 h compared to the hyperlipidemic control group. However, only the group treated with compounds 9, 16 and 18 showed an obviously significant (p | 0.001) reduction in plasma total cholesterol levels after 12 h compared to the hyperlipidemic control group. Moreover, high density lipoprotein
Bezafibrate(Abeita) generic is a fibrate drug, prescribed for high cholesterol in blood. It works mainly by stimulating the action of two enzymes.
Sjögren-Larsson syndrome presents with ichtyosis, spastic diplegia and cognitive deficits. It is caused by a deficiency of fatty aldehyde dehydrogenase. Treatments are limited to symptomatic therapies; for example, ziluteon (an inhibitor of 5-lipoxygenase) can reduce pruritus.. In a recent article, bezafibrate has been shown to induce the expression of the deficient protein in fibroblasts from some patients. This discovery could become of clinical importance ...
The IUPHAR/BPS Guide to Pharmacology. bezafibrate ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
Human CYP2C enzymes metabolize ~30% of clinically prescribed drugs and various environmental chemicals. CYP2C8, an important member of this subfamily, metabolizes the anticancer drug paclitaxel, certain antidiabetic drugs, and endogenous substrates including arachidonic acid to physiologically active epoxyeicosatrienoic acids (EETs). Previous studies from our laboratory showed that microRNA 107 (miR107) and microRNA 103 down-regulate CYP2C8 post-transcriptionally. miR107 is located in intron 5 of the pantothenate kinase 1 (PANK1) gene. p53 has been reported to coregulate the induction of PANK1 and miR107. Here, we examine the possible down regulation of CYP2C8 by drugs capable of inducing miR107. Hypolipidemic drugs such as bezafibrate, known activators of the peroxisome proliferator-activated receptor α (PPARα), induce both the PANK1 gene and miR107 (≈2.5 fold) in primary human hepatocytes. Surprisingly, CYP2C8 mRNA and protein levels were induced by bezafibrate. CYP2C8 promoter activity ...
The aim of this study was to compare the effects of fibrates and omega-3 fatty acids on lymphocyte secretory function and systemic inflammation in patients with isolated hypertriglyceridemia. The stud
Bezalip SR: Bezafibrate belongs to the class of medications known as fibrates. Bezafibrate is used in addition to diet and other measures to treat high cholesterol. It is especially useful in reducing triglycerides, a type of lipid (fat).
Department of Metabolic Regulation, Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine, Matsumoto, Japan (T.N., N.T., H.K., A.H., Y.K., X.Z., T.A.); Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan (N.T., Y.K.); and Laboratory of Metabolism, National Cancer Institute, Bethesda, Maryland (F.J.G ...
The cholesterol drug, taken by six patients with an MTTL1 mutation for 12 weeks, did not induce new mitochondria and raised potential safety concerns.
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SWISS-MODEL Template Library (SMTL) entry for 5x2s.3. Direct Observation of Conformational Population Shifts in Hemoglobin: Crystal Structure of Half-Liganded Hemoglobin after Adding 4 mM bezafibrate pH 6.5.
Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease that eventually leads to end-stage liver failure and death unless liver transplantation (LT) is performed. Ursodeoxycholic acid (UDCA) administered orally at the daily dose of 13-15 mg/kg is currently the only drug approved for the treatment of PBC. UDCA consistently improves biochemical liver tests, prolongs survival without LT, and delays histological progression as well as the occurrence of portal hypertension. However, a significant proportion (40%) of patients treated with UDCA shows an incomplete biochemical response and remains at high risk of death or LT. The development of new treatments in combination with UDCA is therefore needed. Several candidates exist among which is Bezafibrate. Bezafibrate belongs to the fibrates pharmacological class, which has been developed 4 decades ago for the treatment of mixed hyperlipidaemia. Bezafibrate is cheap, widely available and well tolerated. There is now a substantial body of ...
X-linked adrenoleukodystrophy is a devastating peroxisomal disorder with only limited options for treatment. Recent findings however have pointed towards fatty acid elongation as a possible target for therapeutic intervention of X-ALD. Chapter 2 describes how bezafibrate reduces VLCFA levels in X-ALD fibroblasts by inhibiting fatty acid chain elongation. Based on these results, an open-label pilot study was performed to evaluate the effect of bezafibrate on VLCFA accumulation in blood cells of AMN patients. Unfortunately, bezafibrate failed to lower VLCFA levels in blood cells of X-ALD patients. Most likely this is attributable to its inability to reach adequate drug levels in vivo. In chapter 3 the kinetic characteristics of ELOVL1 and further investigation of the effect of fibrates on fatty acid chain elongation are described. This revealed that bezafibrate had the strongest effect in intact cells while the CoA-ester of gemfibrozil was the strongest inhibitor of VLCFA elongation activity in ...
Purpose : Bezafibrate (BZF) is a fibrate drug used as a lipid-lowering agent to treat hyperlipidemia. The results of randomized clinical trial have shown the beneficial effects of systemic fenofibrate therapy in reducing the progression of diabetic retinopathy independently of serum lipid levels. BZF is a pan-agonist for all subtypes of peroxisome proliferator-activated receptor (PPAR) such as PPARα, PPARγ, and PPARβ/δ. It has been reported PPARs play a key role in microvascular inflammation or angiogenesis. However, the effects of BZF in retinal cells remain unclear. The purpose of this study is to investigate the effects of BZF on retinal microvascular inflammation. Methods : The primary human microvascular endothelial cells (HRMECs) and human RPE cell line (ARPE-19) were cultured. First, cytotoxicity and cell viability of BZF were assessed by CCK-8 assay and LDH activity assay. Next, we analyzed the effect of BZF(0,30,100μM) treatment on the expression of TNF-α-induced monocyte ...
Little is known about the relationships between hyperlipidemia and bile acid metabolism. However, hypolipidemic treatment with fibric acid derivatives has been shown to increase biliary cholesterol secretion, presumably by reducing bile acid synthesis. To clarify such relationships, we investigated the effects of different hyperlipoproteinemic conditions and of treatment with fibric acid derivatives on the rates of cholesterol 7 alpha-hydroxylation (the limiting step of bile acid synthesis) in humans. We studied 10 patients (aged 36 to 68 years) with lipoprotein phenotype IIa and with a clinical diagnosis of heterozygous familial hypercholesterolemia, a condition of reduced activity of LDL receptors, and 11 patients (aged 48 to 70 years) with lipoprotein phenotype IIb or IV and clinical diagnosis of familial combined hyperlipidemia, a condition probably related to increased hepatic lipoprotein synthesis. Cholesterol 7 alpha-hydroxylation rates were assayed in vivo by tritium release assay after ...
Here, we describe an investigation, at the lipid, gene, and protein levels, of the effects of the antileukemia and antilymphoma therapy BaP (combined 0.5-mmol/L bezafibrate and 5-μmol/L MPA) on lipogenesis in AML and eBL cells. Our clearest observations on the effects of BaP treatment on lipogenesis in these two disease settings are the following: (i) phospholipid species with saturated and monounsaturated acyl chains were decreased, whereas phospholipids with polyunsaturated chains were increased, (ii) BaP treatment decreased the incorporation of 13C from 13C D-glucose into a variety of cellular lipids, especially into monounsaturated free fatty acids and phospholipids with monounsaturated acyl chains, (iii) BaP caused a decrease in the concentration, and probably the activity, of SCD1, and (iv) supplementation of BaP-treated cells with oleate (the product of SCD1 activity), but not with palmitate, protected AML and eBL cells from killing by BaP. Both bezafibrate and MPA appear to have ...
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In this retrospective cohort study using data of claims, enrolment and health screening, we found that the use of LLDs (statins and fibrates) was associated with an increased risk of new-onset diabetes, compared with non-use. The adjusted HR of new-onset diabetes between two fibrates (bezafibrate and fenofibrate) was similar, while the HR in the high potency statins (atorvastatin, rosuvastatin and pitavastatin) was higher than that in the low potency statins (fluvastatin, pravastatin and simvastatin). The HR for new-onset diabetes was varied from 1.5 to 3.1 in the individual statins. As the incidence rate of new-onset diabetes was estimated as 22.6 per 1000 person-years during the period of non-use in our study, the absolute increase of the rate potentially due to the use of statins, corresponding to HR of 1.5 to 3.1, may be approximately 10 to 45 per 1000 person-years.. Previous studies on the association between the use of statins and new-onset diabetes have been inconclusive. In some of the ...
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This study demonstrates that variation in the PPARα gene influences the onset and progression of type 2 diabetes, in concurrence with the recent observation that bezafibrate reduces the incidence and delays the onset of type 2 diabetes (11). Allele and haplotype frequencies were not different between healthy middle-aged U.K. men and the type 2 diabetes sample, but haplotype frequency was different between subjects with age at diagnosis ≤45 years and both those with later age at diagnosis and with healthy middle-aged U.K. men without overt type 2 diabetes, indicating that PPARα predisposes to early-onset type 2 diabetes. PPARα gene variants influenced age at diagnosis in combination and in haplotype analysis. Carriers of the intron 1 and 7 rare C-alleles had a dramatically younger age at diagnosis, an effect confirmed in haplotype analysis, in which haplotypes 6 and 8, comprising the intron 1 C- and intron 7 C-alleles with the L162 or V162 alleles, respectively, were associated with an age ...
chains in the Genus database with same CATH superfamily 2BZF A; 2EZZ A; 1CI4 A; 2EZY A; 2ODG A; 1QCK A; 2EZX A; #chains in the Genus database with same CATH topology 5J2B A; 3PR5 B; 8ICX A; 4JMU A; 3RRH A; 1BPX A; 5AIB A; 4Y2S A; 5KFN A; 2KHV A; 2RLT A; 1QQ6 A; 1UCV A; 4KIT B; 4P4P A; 2WTF A; 1K1S A; 4KN4 A; 1X6I A; 5KG6 A; 4QIW C; 3PSP A; 1Z1B A; 4M9H A; 5DLF A; 2KFN A; 1AQ6 A; 5ALD A; 4R65 A; 3RR8 A; 5L1K A; 1HUZ A; 1KSP A; 3F5E A; 1ARO P; 3QU5 A; 3RFA A; 2W9A A; 1X9W A; 1ZQJ A; 3D2Q A; 5IIL A; 3HT3 A; 4PHP A; 3RBD A; 4F71 A; 3SEI A; 5AK6 A; 3RJK A; 2XY6 A; 4ECR A; 4B9T A; 1FO4 A; 3SYZ A; 3RH6 A; 2ESE A; 2PMZ F; 2PFO A; 2CRX A; 3BQ7 A; 5KFG A; 3QX7 A; 8ICU A; 1L3U A; 2V4Q A; 2Q0Z X; 4NJ8 A; 9ICK A; 3RB6 A; 7ICL A; 1K5O A; 1ZQG A; 4DQP A; 4UAR A; 5KFA A; 4IQW A; 8ICN A; 8ICI A; 1VJ5 A; 4Y2Q A; 2DQN B; 4DCC A; 1Q3V A; 7ICT A; 5ALG A; 4YFK A; 3AQF A; 2GO7 A; 5AKJ A; 4PPX A; 4KLJ A; 4KLH A; 2ZUD A; 5DBB A; 4J9L A; 3QUT A; 4QWE A; 4QWC A; 2XO7 A; 2JH1 A; 4PL2 A; 4PGY A; 5KFW A; 1TK5 A; 3UQ2 A; 3MR3 ...
Looking for online definition of fibric acids in the Medical Dictionary? fibric acids explanation free. What is fibric acids? Meaning of fibric acids medical term. What does fibric acids mean?
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Peroxisome Proliferator Receptor alpha Agonist drug class usage statistics for the United States (2004 - 2014). Statistics include a comparison of all drugs within the drug class of Peroxisome Proliferator Receptor alpha Agonist.
PPAR agonists are drugs which act upon the peroxisome proliferator-activated receptor. They are used for the treatment of symptoms of the metabolic syndrome, mainly for lowering triglycerides and blood sugar. PPAR-alpha and PPAR-gamma are the molecular targets of a number of marketed drugs. The main classes of PPAR agonists are: PPARα (alpha) is the main target of fibrate drugs, a class of amphipathic carboxylic acids (clofibrate, gemfibrozil, ciprofibrate, bezafibrate, and fenofibrate). They were originally indicated for cholesterol disorders and more recently for disorders that feature high triglycerides. PPARγ (gamma) is the main target of the drug class of thiazolidinediones (TZDs), used in diabetes mellitus and other diseases that feature insulin resistance. It is also mildly activated by certain NSAIDs (such as ibuprofen) and indoles, as well as from a number of natural compounds. Known inhibitors include the experimental agent GW-9662. They are also used in treating hyperlipidaemia in ...
Hydromorphone HCl extended-release tablets (Exalgo) are being studied in clinical trials for the management of moderate to severe pain in opioid-tolerant patients requiring continuous, around-the-clock opioid analgesia for extended lengths of time.7 The FDA has stated that the NDA in its current form is not sufficient for approval of this product. The manufacturers of this agent are in discussions to resolve the details related to the approval of this agent.. Pozen Inc. has begun phase III clinical trials for PA32540, a fixed combination of enteric-coated aspirin 325 mg and immediate-release omeprazole 40 mg.8 PA32540 is being studied for secondary stroke and myocardial infarction prevention in patients at risk for gastric ulcers.. Genentech had hoped to receive approval of rituximab for treating patients with earlier stages of rheumatoid arthritis (RA), but the FDA declined to support wider use of the agent due to the risk of the development of progressive multifocal ...
TY - JOUR. T1 - Bezaitbrate attenuates the increase in blood pressure in fructose-fed rats. AU - Si, Xiaochen. AU - Richey, Joyce M.. AU - Webb, R Clinton. PY - 1997/12/1. Y1 - 1997/12/1. N2 - A high fructose diet induces hypertension (HTN). insulin resistance (InsR), and hypertriglyceridemia (HTG). The sequence of these metabolic abnormalities associated with this dietary regimen remains to be elucidated. We hypothesize that HTG leads tds to the development of HTN and InsR in the fructose-fed animal model. Thus, we evaluated the effects of the lipid-lowering drug bezafibrate (BZFB) on FRU-induced HTN and InsR. Male Sprague Dawley rats were divided into 4 groups and placed on the following diets for five weeks; 60% FRU (n=5). FRU+BZFB (30 mg/kg/days (n=5); regular chow (C) (n=6), and regular chow + BZFB (C+BZFB)) (n=6). The results are summarized below. Groups Blood Pressure (mmHg) Triglyceride (mg/dl) FRU (n=5) 144.4 ± 10 * 130.4 ± 18.* 2 FRU+BZFB (n=S) 126 ± 5 102 ± 37# CB (n=6) 125.5 ± 6 ...
The Miller School study, published in Cell Metabolism, found that increasing the number of mitochondria in muscle was able to delay the onset and slow the progression of the disease in a mouse model of mitochondria myopathy created by Francisca Diaz, Ph.D., research assistant professor of neurology.. Our findings showed that we can boost the function of even a defective mitochondrial enzyme by inducing the production of more mitochondria, says Carlos Moraes, Ph.D., professor of neurology, cell biology and anatomy, and senior author of the study. Its a case of more is better-even a defective mitochondrial enzyme in large numbers is better than a small number.. The researchers were able to increase the mitochondrial levels through genetic overexpression of a master regulator of mitochondrial biogenesis (PGC-1alpha) or by using bezafibrate, a drug already used in humans with high cholesterol.. The fact that we can induce mitochondrial biogenesis with drugs that are already in the marketplace ...
Huang Y, Powers C, Moore V, Schafer C, Ren M, Phoon CK, James JF, Glukhov AV, Javadov S, Vaz FM, Jefferies JL, Strauss AW, Khuchua Z. The PPAR pan-agonist bezafibrate ameliorates cardiomyopathy in a mouse model of Barth syndrome. Orphanet J Rare Dis. 2017 Mar 9;12(1):49. doi: 10.1186/s13023-017-0605-5. (PubMed - Open Access)*. Dudek J, Cheng IF, Chowdhury A, Wozny K, Balleininger M, Reinhold R, Grunau S, Callegari S, Toischer K, Wanders RJ, Hasenfuß G, Brügger B, Guan K, Rehling P. Cardiac-specific succinate dehydrogenase deficiency in Barth syndrome. EMBO Mol Med.2016 Feb 1;8(2):139-54. (PubMed - Open Access)▼. Angelini R, Lobasso S, Gorgoglione R, Bowron A, Steward CG, Corcelli A. Cardiolipin fingerprinting of leukocytes by MALDI-TOF/MS as screening tool for Barth syndrome. J Lipid Res. 2015 Sep;56(9):1787-94. doi: 10.1194/jlr.D059824. Epub 2015 Jul 5. (PubMed - Open Access)*▼. Cadalbert LC, Ghaffar FN, Stevenson D, Bryson S, Vaz FM, Gottlieb E, Strathdee D. Mouse tafazzin is required ...
Tricor is prescribed medicine to treat high cholesterol and high triglyceride levels. This medicine is also called as Fenofibrate. Tricor is connected with the set of drugs called fibric acid derivatives or cholesterol reducing drugs.
Tricor is prescribed medicine to treat high cholesterol and high triglyceride levels. This medicine is also called as Fenofibrate. Tricor is connected with the set of drugs called fibric acid derivatives or cholesterol reducing drugs.
The BFB line is brought to you by us at Flawless, bringing fierce commitment to quality, commitment that you can literally taste through our BFB E liquid. We took huge pride in creating the amazing BFB blends, using some of the best ingredients available out there on the market. Straight Outta The Toaster is one of our
(KudoZ) English to German translation of fibrate class of lipid-regulating agents: XYZ ist die oberste Gruppe von Fibraten der lipidregulierenden Mittel [Medical].
Unter den systemischen Lipidsenkern nehmen die Fibrate einen hervorragenden Platz ein. Mit Clofibrat als Ausgangssubstanz ist diese Stoffgruppe seit gut 20 Jahren in die Therapie der Hyperlipidämien...
It is generally assumed that inflammatory bowel disease (IBD)-related carcinogenesis occurs as a result of chronic inflammation. We previously developed a novel colitis-related mouse colon carcinogenesis model initiated with azoxymethane (AOM) and followed by dextran sodium sulfate (DSS). In the present study we investigated whether a cyclooxygenase (COX)-2 inhibitor nimesulide and ligands for peroxisome proliferator-activated receptors (PPARs), troglitazone (a PPARγ ligand) and bezafibrate (a PPARα ligand) inhibit colitis-related colon carcinogenesis using our model to evaluate the efficacy of these drugs in prevention of IBD-related colon carcinogenesis. Female CD-1 (ICR) mice were given a single intraperitoneal administration of AOM (10 mg/kg body weight) and followed by one-week oral exposure of 2% (w/v) DSS in drinking water, and then maintained on the basal diets mixed with or without nimesulide (0.04%, w/w), troglitazone (0.05%, w/w), and bezafibrate (0.05%, w/w) for 14 weeks. The inhibitory
0174] In some embodiments, the second active is niacin, bezafibrate; ciprofibrate; clofibrate; gemfibrozil; fenofibrate; DF4 (Ac-D-W-F-K-A-F-Y-D-K-V-A-E-K-F-K-E-A-F-NH2); DFS; RVX-208 (Resverlogix); avasimibe; pactimibe sulfate (CS-505); CI-1011 (2,6-diisopropylphenyl[(2,4,6-triisopropylphenyl)acetyl]sulfamate); CI-976 (2,2-dimethyl-N-(2,4,6-trimethoxyphenyl)dodecanamide); VULM1457 (1-(2,6-diisopropyl-phenyl)-3-[4-(4-nitrophenylthio)phenyl]urea); CI-976 (2,2-dimethyl-N-(2,4,6-trimethoxyphenyl)dodecanamide); E-5324 (n-butyl-N-(2-(3-(5-ethyl-4-phenyl-1H-imidazol-1-yl)propoxy)-6-methylphe- nyl)urea); HL-004 (N-(2,6-diisopropylphenyl)tetradecylthioacetamide); KY-455 (N-(4,6-dimethyl-1-pentylindolin-7-yl)-2,2-dimethylpropanamide); FY-087 (N-[2-[N-pentyl-(6,6-dimethyl-2,4-heptadiynyl)amino]ethyl]-(2-met- hyl-1-naphthyl-thio)acetamide); MCC-147 (Mitsubishi Pharma); F 12511 ((S)-2,3,5-trimethyl-4-hydroxy-alpha-dodecylthioacetanilide); SMP-500 (Sumitomo Pharmaceuticals); CL 277082 ...
and the U.S. markets.. Tribute markets Cambia® (diclofenac potassium for oral solution), Bezalip® SR (bezafibrate), Soriatane® (acitretin), NeoVisc® (1.0% sodium hyaluronate solution) Uracyst® (sodium chondroitin sulfate solution 2%), Fiorinal®, Fiorinal® C, Visken®, Viskazide®, Collatamp® G, Durela®, Proferrin®, Iberogast®, MoviPrep®, Normacol®, Resultz®, Pegalax®, Balanse®, Balanse® Kids, Diaflor™, Mutaflor®, and Purfem® in the Canadian market. Additionally, NeoVisc® and Uracyst® are commercially available and are sold globally through various international partnerships. Tribute also has the U.S. rights to Fibricor® and its related authorized generic. In addition, it has the exclusive U.S. rights to develop and commercialize Bezalip® SR in the U.S. and has the exclusive right to sell bilastine, a product licensed from ...
Looking for KETOPROFEN 25, 50, 75, 100, 150, and 200 mg capsules Registered user of Farmavita.Net is looking for EU CTD Dossier with supply for KETOPROFEN 25, 50, 75, 100, 150, and 200 mg capsules. Ketoprofen, (RS)2-(3-benzoylphenyl)-propionic acid (chemical formula C16H14O3) is one of the propionic acid class of non-steroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic effects. It acts by inhibiting the bodys ...
Fibrate Drugs can be effective in treating Lipid Disorders. Learn about Fibrate Drugs, see related evidence, and find other smart treatments for Lipid Disorders at FoundHealth.
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ACE inhibitors, alcohol, and fibrates are among the substances that can negatively interact with Levemir. This eMedTV Web article outlines other medicines that may cause Levemir drug interactions and describes the potential problems that may occur.
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Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), has been generally used to treat ... Bezafibrate improves insulin sensitivity and metabolic flexibility in STZ-treated diabetic mice.. ...
TrOCs for which substantial sorption is possible (venlafaxine, metoprolol, bezafibrate) are amongst the TrOCs which correlate ... metoprolol and bezafibrate18), it can considerably affect DOM availability28. ...
Effects of bezafibrate and fenofibrate on insulin sensitivity in patients with type 2 diabetes mellitus.. Type 2 diabetes ...
Anti-kindling Effect of Bezafibrate, a Peroxisome Proliferator-activated Receptors Alpha Agonist, in Pentylenetetrazole Induced ...
... from the Bezafibrate Infarction Prevention Trial). Author(s): Goldenberg I, Benderly M, Sidi R, Boyko V, Tenenbaum A, et al. ...
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  • Publication Server of Helmholtz Zentrum München: Bezafibrate improves insulin sensitivity and metabolic flexibility in STZ-treated diabetic mice. (helmholtz-muenchen.de)
  • Effects of bezafibrate and fenofibrate on insulin sensitivity in patients with type 2 diabetes mellitus. (umin.ac.jp)