A fibric acid derivative used in the treatment of HYPERLIPOPROTEINEMIA TYPE III and severe HYPERTRIGLYCERIDEMIA. (From Martindale, The Extra Pharmacopoeia, 30th ed, p986)
An antihyperlipoproteinemic agent and uricosuric agent.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
A P450 oxidoreductase that catalyzes the hydroxylation of the terminal carbon of linear hydrocarbons such as octane and FATTY ACIDS in the omega position. The enzyme may also play a role in the oxidation of a variety of structurally unrelated compounds such as XENOBIOTICS, and STEROIDS.
Electron-dense cytoplasmic particles bounded by a single membrane, such as PEROXISOMES; GLYOXYSOMES; and glycosomes.
A class of nongenotoxic CARCINOGENS that induce the production of hepatic PEROXISOMES and induce hepatic neoplasms after long-term administration.
Methylene cyclopropyl alanine and congeners isolated from the unripe edible fruit of the AKEE plant (BLIGHIA SAPIDA). Hypoglycin B is the gamma-glutamyl congener of hypoglycin A. They are very toxic and teratogenic, causing a syndrome called Jamaican vomiting sickness that includes a fall in blood glucose due to the interference of FATTY ACIDS and LEUCINE metabolism which leads to VOMITING, liver damage, CONVULSIONS and DEATH.
A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
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.
An oral hypolipemic agent primarily used in DOGS and RATS.
A powerful herbicide used as a selective weed killer.
An enzyme that catalyzes the formation of O-acetylcarnitine from acetyl-CoA plus carnitine. EC 2.3.1.7.
An ester of phthalic acid. It appears as a light-colored, odorless liquid and is used as a plasticizer for many resins and elastomers.
A strongly basic anion exchange resin whose main constituent is polystyrene trimethylbenzylammonium Cl(-) anion.
A plant genus of the family ARECACEAE. It is a tropical palm tree that yields a large, edible hard-shelled fruit from which oil and fiber are also obtained.
Substances used to lower plasma CHOLESTEROL levels.
An antilipemic agent that lowers CHOLESTEROL and TRIGLYCERIDES. It decreases LOW DENSITY LIPOPROTEINS and increases HIGH DENSITY LIPOPROTEINS.
Treatment of disease by exposure to light, especially by variously concentrated light rays or specific wavelengths.
An enzyme that catalyzes the first and rate-determining steps of peroxisomal beta-oxidation of fatty acids. It acts on COENZYME A derivatives of fatty acids with chain lengths from 8 to 18, using FLAVIN-ADENINE DINUCLEOTIDE as a cofactor.
The process that starts the transcription of an RNA molecule. It includes the assembly of the initiation complex and establishment of the start site.
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.
An increase in the rate of synthesis of an enzyme due to the presence of an inducer which acts to derepress the gene responsible for enzyme synthesis.
Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.
A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, and chemicals from the environment.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent.
Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.
A test to determine the ability of an individual to maintain HOMEOSTASIS of BLOOD GLUCOSE. It includes measuring blood glucose levels in a fasting state, and at prescribed intervals before and after oral glucose intake (75 or 100 g) or intravenous infusion (0.5 g/kg).
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.
Glucose in blood.
A phenolphthalein that is used as a diagnostic aid in hepatic function determination.
An enzyme that catalyzes the transfer of methyl groups from S-adenosylmethionine to free carboxyl groups of a protein molecule forming methyl esters. EC 2.1.1.-.
A plant genus in the family Boraginaceae, order Lamiales, subclass Asteridae. This is the True Heliotrope that should not be confused with an unrelated plant sometimes called Garden Heliotrope (VALERIAN).
A plant genus of the family RUBIACEAE. Members contain genepin, from which geniposide is obtained for use as a crosslinking agent in ADHESIVES, and 3-caffeoyl-4-sinapoylquinic acid.
A flavoprotein containing oxidoreductase that catalyzes the dehydrogenation of SUCCINATE to fumarate. In most eukaryotic organisms this enzyme is a component of mitochondrial electron transport complex II.
Mitochondria in hepatocytes. As in all mitochondria, there are an outer membrane and an inner membrane, together creating two separate mitochondrial compartments: the internal matrix space and a much narrower intermembrane space. In the liver mitochondrion, an estimated 67% of the total mitochondrial proteins is located in the matrix. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p343-4)
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds.
Inorganic salts of the hypothetical acid, H3Fe(CN)6.
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
A branch of genetics which deals with the genetic variability in individual responses to drugs and drug metabolism (BIOTRANSFORMATION).
Inorganic compounds that contain aluminum as an integral part of the molecule.
A compound with many biomedical applications: as a gastric antacid, an antiperspirant, in dentifrices, as an emulsifier, as an adjuvant in bacterins and vaccines, in water purification, etc.
Detection of a MUTATION; GENOTYPE; KARYOTYPE; or specific ALLELES associated with genetic traits, heritable diseases, or predisposition to a disease, or that may lead to the disease in descendants. It includes prenatal genetic testing.
The systematic study of the complete DNA sequences (GENOME) of organisms.
A strong acid used as a protein precipitant in clinical chemistry and also as a caustic for removing warts.
Salts and esters of the 16-carbon saturated monocarboxylic acid--palmitic acid.
The separation of particles from a suspension by passage through a filter with very fine pores. In ultrafiltration the separation is accomplished by convective transport; in DIALYSIS separation relies instead upon differential diffusion. Ultrafiltration occurs naturally and is a laboratory procedure. Artificial ultrafiltration of the blood is referred to as HEMOFILTRATION or HEMODIAFILTRATION (if combined with HEMODIALYSIS).
Refuse liquid or waste matter carried off by sewers.
A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids.
Arginine derivative which is a substrate for many proteolytic enzymes. As a substrate for the esterase from the first component of complement, it inhibits the action of C(l) on C(4).
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.

Comparison of the stability and substrate specificity of purified peroxisomal 3-oxoacyl-CoA thiolases A and B from rat liver. (1/434)

The specific activities and substrate specificities of 3-oxoacyl-CoA thiolase A (thiolase A) purified from normal rat liver peroxisomes and 3-oxoacyl-CoA thiolase B (thiolase B) isolated from livers of rats treated with the peroxisome proliferator clofibrate were virtually identical. The enzymes could be distinguished by their N-terminal amino acid sequences, their isoelectric points and their stability, the latter being higher for thiolase A. Contrary to thiolase B, which showed a marked cold lability in the presence of KCl by dissociating into monomers with poor activity, thiolase A retained its full activity and its homodimeric structure under these conditions.  (+info)

Preventive effects of dehydroepiandrosterone acetate on the fatty liver induced by orotic acid in male rats. (2/434)

Preventive effects of dehydroepiandrosteone acetate (DHEA-A) and clofibrate (positive control substance) on the fatty liver induced by orotic acid (OA) were examined on the male Sprague-Dawley rats fed a high sucrose based diet containing 1% OA and this diet further mixed with 0.5% DHEA-A or 0.5% clofibrate for 2 weeks. Numerous lipid droplets were observed in the hepatocytes of the rats treated with OA alone, but not in those treated with DHEA-A or clofibrate. In comparison to the group with OA alone, the DHEA-A or clofibrate treated rats showed a larger relative liver weight (to body weight) which was accompanied by increased peroxisomes in the hepatocytes. These results indicate that DHEA-A, as well as clofibrate, may prevent OA-induced fatty liver.  (+info)

Cellular distribution of cytochromes P-450 in the rat kidney. (3/434)

The distribution of several cytochrome P-450 (P-450) isoenzymes between proximal tubular (PT) and distal tubular (DT) cells of the rat kidney was determined. Western blot analysis of microsomes prepared from liver and kidney cortical homogenates revealed that CYP2E1 protein was expressed in rat kidney microsomes at approximately 10% of hepatic levels. Microsomes from renal cortical, PT, and DT cells all expressed CYP2E1, with DT microsomes expressing slightly higher levels than PT microsomes. In contrast, chlorzoxazone hydroxylation activity was markedly higher in microsomes from PT cells than in those from DT cells. Northern blot analysis of total RNA from PT and DT cells exhibited a pattern of CYP2E1 mRNA distribution similar to that of CYP2E1 protein. CYP2C11 protein expression in renal cortical microsomes was approximately 10% of that in liver microsomes but was significantly higher in microsomes from PT cells than in those from DT cells. CYP3A1/2 was not detected in microsomes from either cortical, PT, or DT cells, but was detected in microsomes isolated from total liver or kidney cortical homogenates. CYP2B1/2 expression was detected in all tissues tested. The peroxisomal proliferator clofibrate enhanced the level of CYP2B1/2 in microsomes from both total liver and kidney cortical homogenates but not in microsomes from cortical, PT, or DT cells. CYP4A2/3 protein and CYP4A mRNA expression were detected in microsomes from total liver and kidney cortical homogenates and from renal cortical, PT, and DT cells using Western and Northern blot analyses, respectively. Lauric acid hydroxylation activity, an indicator of CYP4A, was comparable in PT and DT cells. Clofibrate elevation of CYP4A in cortical, PT, and DT microsomes was not as great as that detected in total kidney cortical microsomes. These results establish the distribution of several P-450 isoenzymes between different cell populations of the rat kidney. Furthermore, these results present evidence that the level of induction of certain P-450 isoenzymes in the kidney is cell type-specific.  (+info)

Effect of gemfibrozil in vitro on fat-mobilizing lipolysis in human adipose tissue. (4/434)

Fat-mobilizing lipolysis was studied in rat and human adipose tissue during incubation in vitro by following the release of glycerol into the incubation medium. Gemfibrozil as well as clofibrate consistently and readily inhibited basal as well as noradrenaline-stimulated fat-mobilizing lipolysis in rat fat. With human adipose tissue no effect was observed with gemfibrozil and clofibrate on basal lipolysis. This may be due to the comparatively low rate of the nonstimulated fat-mobilizing lipolysis in human tissue incubated in vitro. When lipolysis was stimulated with noradrenaline as well as isoprenaline, however, both gemfibrozil and clofibrate significantly reduced the fat-mobilizing lipolysis. This inhibition of lipolysis was however not observed in all studies. When lipolysis had been stimulated with theophylline, no inhibition of lipolysis was obtained with either compound. The possibility that reduced fat-mobilizing lipolysis in adipose tissue may cause a lowering of plasma triglycerides by reducing the flow of FFA to the liver is discussed in some detail. It is also suggested that inhibition of lipolysis may be accompanied by increased activity of lipoprotein lipase as well as an increase in the FIAT process. However, the pharmacological implication of the above-mentioned findings, particularly for gemfibrozil, must await further studies, as fairly large doses, around 1 mg/ml of incubation medium, were needed to obtain inhibition of fat-mobilizing lipolysis.  (+info)

Inhibition of transforming growth factor beta1-induced hepatoma cell apoptosis by liver tumor promoters: characterization of primary signaling events and effects on CPP32-like caspase activity. (5/434)

The effects of the liver tumor promoters phenobarbital, clofibrate, dieldrin, and DDT on transforming growth factor-beta1 (TGFbeta)-induced apoptosis were studied in FTO-2B hepatoma cells. Inhibition of apoptosis by these compounds was strongly correlated with a decrease in CPP32-like caspase activity. Similar effects were obtained with insulin and dexamethasone. CPP32-like activity may thus provide a useful tool for quantiation of apoptosis under various treatment conditions. Diverse effects on apoptosis-associated cellular signaling proteins were observed: insulin led to an activation of the MAP kinases ERK1/2, of PKB/Akt and of NF-kappaB, phenobarbital and clofibrate enhanced NF-kappaB activity solely, while dexamethasone slightly enhanced NF-kappaB activity and increased the expression of Bcl-xL. Since inhibition of apoptosis was still detectable if the anti-apoptotic compounds were administered more than 10 h after TGFbeta, the diverse primary signals appear to converge at a presumably late stage of apoptosis, but upstream of activation of CPP32 or related caspases.  (+info)

Fibrates suppress fibrinogen gene expression in rodents via activation of the peroxisome proliferator-activated receptor-alpha. (6/434)

Plasma fibrinogen levels have been identified as an important risk factor for cardiovascular diseases. Among the few compounds known to lower circulating fibrinogen levels in humans are certain fibrates. We have studied the regulation of fibrinogen gene expression by fibrates in rodents. Treatment of adult male rats with fenofibrate (0.5% [wt/wt] in the diet) for 7 days decreased hepatic Aalpha-, Bbeta-, and gamma-chain mRNA levels to 52% +/- 7%, 46% +/- 8%, and 81% +/- 19% of control values, respectively. In parallel, plasma fibrinogen concentrations were decreased to 63% +/- 7% of controls. The suppression of fibrinogen expression was dose-dependent and was already evident after 1 day at the highest dose of fenofibrate tested (0.5% [wt/wt]). Nuclear run-on experiments showed that the decrease in fibrinogen expression after fenofibrate occurred at the transcriptional level, as exemplified for the gene for the Aalpha-chain. Other fibrates tested showed similar effects on fibrinogen expression and transcription. The effect of fibrates is specific for peroxisome proliferator-activated receptor-alpha (PPARalpha) because a high-affinity ligand for PPARgamma, the thiazolidinedione BRL 49653, lowered triglyceride levels, but was unable to suppress fibrinogen expression. Direct evidence for the involvement of PPARalpha in the suppression of fibrinogen by fibrates was obtained using PPARalpha-null (-/-) mice. Compared with (+/+) mice, plasma fibrinogen levels in (-/-) mice were significantly higher (3.20 +/- 0.48 v 2.67 +/- 0.42 g/L). Also, hepatic fibrinogen Aalpha-chain mRNA levels were 25% +/- 11% higher in the (-/-) mice. On treatment with 0.2% (wt/wt) fenofibrate, a significant decrease in plasma fibrinogen to 77% +/- 10% of control levels and in hepatic fibrinogen Aalpha-chain mRNA levels to 65% +/- 12% of control levels was seen in (+/+) mice, but not in (-/-) mice. These studies show that PPARalpha regulates basal levels of plasma fibrinogen and establish that fibrate-suppressed expression of fibrinogen in rodents is mediated through PPARalpha.  (+info)

The effect of peroxisome proliferators on mitochondrial bioenergetics. (7/434)

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)

Hypoxia-induced production of 12-hydroxyeicosanoids in the corneal epithelium: involvement of a cytochrome P-4504B1 isoform. (8/434)

The corneal epithelium metabolizes arachidonic acid by a cytochrome P-450 (CYP)-mediated activity to 12-hydroxy-5,8,11, 14-eicosatetraenoic acid (12(R)-HETE) and 12-hydroxy-5,8, 14-eicosatrienoic acid (12(R)-HETrE ). Both metabolites possess potent inflammatory properties, with 12(R)-HETrE being a powerful angiogenic factor, and they assume the role of inflammatory mediators in hypoxia- and chemical-induced injury in the cornea in vivo and in vitro. We used a model of corneal organ culture that exhibits hypoxia-induced epithelial CYP-dependent 12(R)-HETE and 12(R)-HETrE synthesis for isolating, identifying, and characterizing the CYP protein responsible for these eicosanoid syntheses. Northern analysis revealed the presence of a CYP4A-hybridizable mRNA, the levels of which were increased after hypoxia. Reverse transcription-polymerase chain reaction analysis with primers specific for the CYP4A family led to the isolation of a 671-base pair fragment with a 98.8% sequence homology to the rabbit lung CYP4B1 isoform, of which the levels in the corneal epithelium were greatly increased under hypoxic conditions. Moreover, phenobarbital, an inducer of hepatic CYP4B1 in the rabbit, also induced 12-HETE and 12-HETrE synthesis. Antibodies against CYP4B1, but not against CYP4A1, inhibited hypoxia-, clofibrate-, and phenobarbital-induced 12-HETE and 12-HETrE synthesis. These results suggest the involvement of a CYP4B1 isoform in the corneal epithelial synthesis of these eicosanoids in response to hypoxia.  (+info)

We previously showed that the oxidation of branched-chain amino acids is increased in rats treated with clofibrate [Paul and Adibi (1980) J. Clin. Invest. 65, 1285-1293]. Two subsequent studies have reported contradictory results regarding the effect of clofibrate treatment on gene expression of branched-chain keto acid dehydrogenase (BCKDH) in rat liver. Furthermore, there has been no previous study of the effect of clofibrate treatment on gene expression of BCKDH kinase, which regulates the activity of BCKDH by phosphorylation. The purpose of the present study was to investigate the above issues. Clofibrate treatment for 2 weeks resulted in (a) a 3-fold increase in the flux through BCKDH in mitochondria isolated from rat liver, and (b) a modest but significant increase in the activity of BCKDH. However, clofibrate treatment had no significant effect on the mass of E1α, E1β, and E2 subunits of BCKDH or the abundance of mRNAs encoding these subunits. On the other hand, clofibrate treatment ...
Whole cells, homogenates and mitochondrial obtained from the livers of albino rats which were starved for 6 days or more showed a 50% decrease in oxidative activity. The decrease could be corrected by the addition of cytochrome c in vitro. The phosphorylative activity of mitochondria remained unaffected. The decrease in oxidative rate was not observed when starving animals were given the anti-hypercholesterolaemic drug clofibrate. The total cellular concentration of cytochrome c was not affected by starvation. However, the concentration of the pigment in hepatic mitochondria isolated from starving animals was less than half that in normal mitochondria. Clofibrate-treated animals did not show a decreased concentration of cytochrome c in hepatic mitochondria. Mitochondria isolated from starving animals, though deficient in cytochrome c, did not show any decrease in succinate dehydrogenase activity or in the rate of substrate-dependent reduction of potassium ferricyanide or attendant ...
Pretreatment of mice with the peroxisome proliferator clofibrate (CFB) protects against acetaminophen (APAP)-induced hepatotoxicity. Previous studies have shown that activation of the nuclear peroxisome proliferator activated receptor-alpha (PPARalpha) is required for this effect. The present study …
Clofibrate is an antilipidemic agent similar to gemfibrozil. It acts to lower elevated serum lipids by reducing the very low-density lipoprotein fraction (Sf 20-400) rich in triglycerides. Serum cholesterol may be decreased, particularly in those patients whose cholesterol elevation is due to the presence of IDL as a result of Type III hyperlipoproteinemia. Several investigators have observed in their studies that clofibrate may produce a decrease in cholesterol linoleate but an increase in palmitoleate and oleate, the latter being considered atherogenic in experimental animals. The significance of this finding is unknown at this time. Reduction of triglycerides in some patients treated with clofibrate or certain of its chemically and clinically similar analogs may be associated with an increase in LDL cholesterol. Increase in LDL cholesterol has been observed in patients whose cholesterol is initially normal. Animal studies suggest that clofibrate interrupts cholesterol biosynthesis prior to ...
Clofibrate is an antilipidemic agent similar to gemfibrozil. It acts to lower elevated serum lipids by reducing the very low-density lipoprotein fraction (Sf 20-400) rich in triglycerides. Serum cholesterol may be decreased, particularly in those patients whose cholesterol elevation is due to the presence of IDL as a result of Type III hyperlipoproteinemia. Several investigators have observed in their studies that clofibrate may produce a decrease in cholesterol linoleate but an increase in palmitoleate and oleate, the latter being considered atherogenic in experimental animals. The significance of this finding is unknown at this time. Reduction of triglycerides in some patients treated with clofibrate or certain of its chemically and clinically similar analogs may be associated with an increase in LDL cholesterol. Increase in LDL cholesterol has been observed in patients whose cholesterol is initially normal. Animal studies suggest that clofibrate interrupts cholesterol biosynthesis prior to ...
Innovative genomic test for aluminium clofibrate personalised pharmacogenomic analysis to explore how your genes can affect and modulate your response ...
Line p2h3-18-3. Expressed in all tissues. Expression is weak in the outer tissues in the mature part of the root but it remains high in the vascular tissues.. ...
Campus Assaults, a piercing, monumental exposé of rape culture on campuses, poised to light a fire under a national debate.. In a tour de force of verité footage, expert insights, and first-person testimonies, the film follows undergraduate rape survivors pursuing both their education and justice, despite ongoing harassment and the devastating toll on them and their families.. Scrutinizing the gamut of elite Ivies, state universities, and small colleges, filmmakers Kirby Dick and Amy Ziering reveal an endemic system of institutional cover-ups, rationalizations, victim-blaming, and denial that creates perfect storm conditions for predators to prey with impunity.. Meanwhile, the film captures mavericks Andrea Pino and Annie Clark, survivors who are taking matters into their own hands-ingeniously employing Title IX legal strategy to fight back and sharing their knowledge among a growing, unstoppable network of young women who will no longer be silent.. Since the films premiere at Sundance, it ...
Pharmaceuticals in the aquatic environment is an emerging issue and the risks they pose are mostly unknown. They are used in large amounts throughout the world and can enter the environment, as the active metabolite or unmetabolised, through excretion by people and improper disposal. As these drugs are designed to have specific biological effects in a specific organism (as well as sometimes having other non-specific side effects), their potential to cause effects within the environment is great. Clofibric acid (the major metabolite of the lipid lowering drug, Clofibrate) is non-biodegradable, highly motile, very persistent and frequently detected at μg/I levels in the environment. I studied possible effects of clofibric acid in fish, using different experimental approaches and endpoints. The studies involve two different species, and for one of these species, fish at different stages of development. The chapters within this thesis have presented the first evidence (albeit preliminary) of ...
The isolation and purification of two major phenobarbitone-induced hepatic cytochromes P-450 from male Wistar rats is described. These forms (designated cytochromes P-450 B1 and P-450 B2) were extensively characterised and structurally and functionally compared to two other homogeneous isoenzymic forms, cytochromes P-452 (clofibrate-induced) and cytochrome P-447 (BNF-induced). These characterisation studies (including catalytic, immunological, physical and spectral analysis) indicated that all four isoenzymes were distinct, unique hemoproteins. The above characterisation was extended towards the induction profiles of these hemoproteins in hepatic and renal microsomes, following single dose xenobiotic pretreatment. Of primary interest was the immunoquantitation data which revealed the presence of cytochrome P-452 as a major constitutive isoenzyme. This data in conjunction with the metabolic data also indicated that xenobiotic induction of cytochromes P-450 was both a specific and precise event. ...
Effects of Puer Tea:1.Decrease the blood fat, lose weight, decline blood pressure and resist arteriosclerosis.Dr. Amill Carroby, from a college of Paris, French used Yunnan Puer Tuo tea to do clinical trial and proved that: Yunnan Puer Tea has a good effect to reduce content of lipoid and cholesterol. Kunming Medical College of China also observed 55 clinical trials to use Yunnan Puer Tuo tea to cure the high blood fat diseases and compare them with 31 cases used clofibrate which has a good effect to incline fat. The result shows that the curative effect of Puer Tea is higher than clofibrate. Long lasting drinkers of Puer Tea can reduce cholesterol and glycerin fat. So long drinking of Puer Tea can have the effect of curative the obesity. Drinking of Puer tea can cause physiological effect in stretching human beings blood vessel, descending blood pressure and slowering the rhythm of the heart, etc. So it has a good curative function to high blood pressure and the brain ...
Thank you for your interest in spreading the word about Diabetes Care.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...
Fenofibrate (isopropyl 4-( p-chlorobenzoyl)phenoxyisobutyrate: Lipanthyl) is a hypolipidaemic agent structurally related to Clofibrate. In view of current concern over the safety-in-use of this class...
The existence of interactions between retinoids and P450 and GT systems is well established; retinoids both affect and are metabolized by these systems. The potential for the metabolism of retinoids to be affected by alterations in P450 and GT enzyme levels (caused by pretreatment with either themselves or other drugs) is demonstrated by the induction of the P450-mediated metabolism of ATRA by dexamethasone and phenobarbital (Martini and Murray, 1994) and the induction of the glucuronidation of ATRA by 3-methylcholanthrene and clofibrate (Genchiet al., 1996; Sass et al., 1994). In addition, P450 inhibitors have been shown to prolong the in vivohalf-life of ATRA in rats (Van Wauwe et al., 1988, 1990) and mice (Achkar et al., 1994). Therefore, the potential for drug-drug interactions, as well as alterations in their own metabolism after repeated administration, is clearly evident for the retinoids. However, very little is known about either the nature of the effects of retinoids on these metabolic ...
membranes forex analysis for today Hypolipidemic - forex analysis for today, day forex system trading, global forex trading offers
Despite the importance of Arctic and boreal regions in the present carbon cycle, estimates of annual high-latitude carbon fluxes vary in sign and magnitude. Without accurate estimates of current carbon fluxes from Arctic and boreal ecosystems, predicting the response of these systems to global change is daunting. A number of factors control carbon turnover in high-latitude soils, but because they are unique to northern systems, they are mostly ignored by biogeochemical models used to predict the response of these systems to global change. Here, we review those factors. First, many northern systems are dominated by mosses, whose extremely slow decomposition is not predicted by commonly used indices of litter quality. Second, cold temperature, permafrost, waterlogging, and substrate quality interact to stabilize soil organic matter, but the relative importance of these factors, and how they respond to climate change, is unknown. Third, recent evidence suggests that biological activity occurring ...
Coronaviruses encompass a large family of viruses that cause the common cold as well as more serious diseases, such as the ongoing outbreak of coronavirus disease 2019 (COVID-19; formally known as 2019-nCoV). Coronaviruses can spread from animals to humans; symptoms include fever, cough, shortness of breath, and breathing difficulties; in more severe cases, infection can lead to death. This feed covers recent research on COVID-19. ...
They do not an sVT somatostatin which can cause first-dose hypotension. Little or severe attack subsequently interacts with one of glaucoma. It may be useful member of ingestion of coronary heart, and blurred vision. He was managed without cilastatin, such as well Ezetimibe is upper gastro-intestinal disturbances Life-threatening bleeding, as megestrol. He was managed without cilastatin, such as well Ezetimibe is upper gastro-intestinal disturbances. Some patients with a combination with isoniazid is administered intravenously. The european following perforation and is generally unproven Defective. Trace element deficiencies can provoke encephalopathy should be given as it causes arousal and hypotension can be obtained. Headache, because the baby she started well and may be attributed to the urine output. Useful websites: american previously uninfected cD4/CCR5-positive following general :public. Therefore pregnant women with clofibrate may be necessary intravenously followed by depot ...
We offer fully characterized, pooled microsomes and S9 from Sprague-Dawley® rat tissue that has been treated with different chemical enzyme inducers, including the following: Aroclor 1254 B-Naphthoflavone Clofibrate Dexamethasone Isoniazid 3-Methylcholanthrene Phenobarbital Individual and pooled human S9 have been produced from a bank of different human livers, enabling you to use these products to predict the
Acid phosphatase is an enzyme present in the cells throughout the body. It is present in especially high concentrations in the prostate and semen in men. Prostatic diseases result in its release in the blood. A blood test can measure the enzyme acid phosphatase. Drugs and substances that can interfere with the test include fluorides, oxalates, clofibrate, and alcohol. ...
Ecobell Topical Shader 25 g, waterproof hair. Ecobell Topical Shader 25 g, waterproof hair concealer. can use Ecobell Topical Shader with Rogaine, Propecia or.Le Romarin aussi efficace que du minoxidil? jojo k-ri. Profil:. patients returned to the clinic for efficacy and safety evaluations every 3 months.Find great deals on eBay for rogaine 5% 12 month and rogaine 5%. Shop with confidence.. Propecia generic vs brand. Buy diclofenac tablets online Mevacor is also who suffer to fight other and clofibrate, the adverse findings with times when it so the ...
To get these sample movies, I began by using the easy confocal microscope. To convey what is at stake here, I will digress to talk a little about fluorescence microscopy in general and the confocal in particular. Fluorescence microscopy is hugely popular today, and by popular I mean used a lot. The reason is because fluorescence is intrinsically high contrast. Contrast means the difference between the thing you are interested in seeing and the background. Stars do not go away during the day, they are simply not contrasted because the difference in intensity between their light and the light from the sun bouncing around the atmosphere is too small. In regular microscopy (which is called bright-field), the background is bright and things you are interested in, say a chloroplast, absorb or scatter light and so they are a little less bright. In contrast, in fluorescence, the background is dark as the night sky, and objects you are interested fluoresce. It turns out that our eyes use the ratio ...
1. Seven subjects were studied before and after the rate of cholesterol synthesis was altered with drugs or dietary cholesterol.. 2. The rate at which plasma free cholesterol was formed from squalene during constant infusions of radioactive mevalonate increased with colestipol treatment, decreased with clofibrate treatment and decreased when cholesterol was added to the diet. The plasma squalene concentration showed corresponding changes, confirming that its measurement may qualitatively define changes in cholesterol synthesis.. 3. The mean plasma squalene concentration in seven hypertriglyceridaemic, slightly overweight subjects was significantly higher than in six hypercholesterolaemic subjects, which is consistent with other evidence for increased cholesterol synthesis in hypertriglyceridaemia. ...
Hughes JL, Poulos A, Robertson E, Chow CW, Sheffield LJ, Christodoulou J, Carter RF. Pathology of hepatic peroxisomes and mitochondria in patients with peroxisomal disorders. Virchows Archiv. A, Pathological anatomy and histopathology 416 (3) : 255 - 64(1990) PubMed ...
PEROXISOME PROLIFERATION DINP is in a class of chemicals known as peroxisome proliferators - chemicals that induce an increase in the size and number of a subcellular organelle known as a peroxisome in the liver cells of rodents. Many peroxisome proliferators are known to cause liver tumors in rodents. As observed with peroxisome proliferators, including DINP, rats and mice are susceptible to the morphological, biochemical, and carcinogenic effects of peroxisome proliferators, while non-human primates and humans are completely non-responsive or refractory. Criteria have been established by IARC to make the determination that tumors resultant from peroxisomal proliferation are not relevant to humans (IARC, 1995 at 12-13): (a) Information is available to exclude mechanisms of carcinogenesis other than those related to peroxisome proliferation. (b) Peroxisome proliferation (increases in peroxisome volume density or fatty acid b-oxidation activity) and hepatocellular proliferation have been ...
Pretreatment with clofibrate (CFB) and other peroxisome proliferators (PPs) confers resistance to acetaminophen (APAP) hepatotoxicity in mice. Previous studies have excluded the involvement of changes in APAP biotransformation and hepatic glutathione (GSH) content in this hepatoprotection model. The work presented here further explored the mechanisms underlying this drug interaction. Many hepatic effects of PPs have been determined to be receptor-mediated. Initial studies showed that peroxisome proliferator-activated receptor α (PPARα)-null mice exposed to CFB are not resistant to APAP hepatotoxicity. This documents that hepatoprotection by CFB is PPARα-dependent and that increased expression of gene products regulated by this receptor may lead to this response. Generation of reactive oxygen species (ROS) and oxidative damage play important roles in APAP hepatotoxicity. Exposure to PPs moderately increases the H2O2-degrading activity of catalase. To determine whether elevated catalase activity
Our study demonstrates that the antihyperlipidemic clofibrate derivatives, which are structurally different from the known activator, sulfobromophthalein, exert stimulatory effects specifically on AKR 1C4 of human liver 3αHSD isoforms. For the activation by sulfobromophthalein, there has been no direct information about the structurally specific interaction between the molecule and the enzyme, except for its sulfonyl group(s) (Matsuura et al., 1996,1997). Our results of the comparative study of the efficacy of the antihyperlipidemic drugs and their related compounds provide the following specific structural requisites for the activator. 1) The existence of a negatively charged carboxyl group, together with at least a hydrophobic aromatic ring, in the activator molecule is necessary to interact with the activator site of the enzyme, because the clofibric acid derivatives lacking the free carboxyl group or the aromatic ring did not activate. Because the pKa values of the carboxyl group of the ...
The role of cholesterol in the development of cardiovascular disease was elucidated in the second half of the 20th century.[138] This lipid hypothesis prompted attempts to reduce cardiovascular disease burden by lowering cholesterol. Treatment consisted mainly of dietary measures, such as a low-fat diet, and poorly tolerated medicines, such as clofibrate, cholestyramine, and nicotinic acid. Cholesterol researcher Daniel Steinberg writes that while the Coronary Primary Prevention Trial of 1984 demonstrated cholesterol lowering could significantly reduce the risk of heart attacks and angina, physicians, including cardiologists, remained largely unconvinced.[139] Scientists in academic settings and the pharmaceutical industry began trying to develop a drug to reduce cholesterol more effectively. There were several potential targets, with 30 steps in the synthesis of cholesterol from acetyl-coenzyme A.[140] In 1971, Akira Endo, a Japanese biochemist working for the pharmaceutical company Sankyo, ...
A lipid intervention clinic screened 4000 employees (89% participation) and identified 150 type IV subjects (top 5 percentile triglyceride values, 100% initial participation, 6% drop out). The 150 healthy type IV subjects, ages 20 to 49, were randomly divided into treatment subgroups: A, treatment by clinic nutritionist and physician with the National Heart and Lung Institutes type IV diet for 6 weeks, then diet plus Clofibrate for 18 weeks; B, same treatment by private physician; C, no intervention for 24 weeks, subjects advised of abnormality. The group A mean fasting serum triglyceride of 407 mg/dl declined 50% at 6 weeks, 61% at 12 weeks, and was unchanged at 24 weeks (P , 0.0005 at 6, 12, 24 weeks). Group B triglyceride decreased 42%, 50%, 41% (P , 0.0005 at 6, 12, 24 weeks). Group C triglyceride declined 20%, 1st to 24th week. Body weight decreased 8% (A) and 4% (B) at 6 weeks (P , 0.0005) and was unchanged at 24 weeks. The maximum cholesterol decrease (A) was 11% (P , 0.0005). Type IV ...
ENCODES a protein that exhibits calcium ion binding; INVOLVED IN calcium ion homeostasis; endoplasmic reticulum organization; ER overload response; ASSOCIATED WITH abnormal cell physiology; increased fibroblast apoptosis; neonatal lethality, complete penetrance; ASSOCIATED WITH Smith-Magenis Syndrome (ortholog); FOUND IN endoplasmic reticulum; rough endoplasmic reticulum; INTERACTS WITH 3,4-methylenedioxymethamphetamine; carbon nanotube; clofibrate
The lack of beneficial effects indicates that the interventions did not work as intended in the included trials. There are several possible explanations for this. Most of the trials were old and consequently used treatments different from what would be used today-such as clofibrate or nicotinic acid for hypercholesterolaemia, instead of statins. Also, thresholds for treating cardiovascular risk factors were higher than they are today. However, it is not a given that the results would be better today, as medical innovations sometimes prove harmful29 and as reducing risk factor thresholds means treating people at lower risk who have a smaller potential for benefit but the same risk of harm.30 Another possibility is that preventive drugs could have a less favourable balance between benefits and harms when used in general populations compared with in pharmacological trials, which often use many exclusion criteria.31 In our meta-analyses, arranged by year of trial start, there are no visible time ...
Statins and other anti-cholesterol drugs The statins (or HMG-CoA reductase inhibitors) along with other drugs, such as cholestyramine (Questran), comprise the class of hypolipidemic drugs. Hypolipidemic drugs are prescribed - sometimes aggressively so - to lower cholesterolStatinsstatinsstatinsstatinsMarshall ProtocolStatinsOlmesartanOlmesartanOlmesartanstatinsNuclear ReceptorsOlmesartanOlmesartancholesterolcholesterolcholesterolstatinscholesterolstatinscholesterolstatinscholesterolcholesterols…
We used an E. coli model iJR904 obtained from BiGG database as a starting model and obtained a growth rate represented by the f value of 0.9129. We then deleted the reaction which encodes for the sulphite reduction pathway and obtained a f value of -8.63e-13 indicating that the sulphite reduction pathway is essential. We wrote a program which finds all essential reactions in M. tuberculosis and E. coli SBML models and attempts to restore growth for each essential E. coli model with essential reactions from M. tuberculosis to identify other metabolic pathways we could apply a targeted drug screen to. We identified 100 other essential reactions we can target.. ...
I am trying to find information on a plant extract known in India as gugulipid. It is an extract of gum gugulu but I have know idea what the plant is called. This is a potent hypolipidemic agent and lowers cholesterol in the blood. It would be a great alternative to the drugs currently on the market which many people have trouble taking. Anyone with any additional info please email me thanks ...
Featuring mycology lessons, essays, and mushroom photographs and descriptions by Dianna Smith and a series of mycology articles by Bill Bakaitis. ...
Findings: All 90 infants enrolled in our study had received phototherapy. The infants were divided into Clofibrate group (G1) consisting of 26 boys (57.8%) and 19 girls (42.2%) and Control group with 24 boys (53.3%) and 21 girls (46.7%) (G2). There were no statistically overt differences between the two groups regarding sex distribution, age, weight and total serum bilirubin level at admission. Mean values for total bilirubin of serum in Clofibrate group 12, 24, 36, and 48 hours after admission were significantly lower than those for Control group ( ...
Reactivity: Human - Sample Type: Cell Culture Supernatant, Plasma. | Order Peroxisome Proliferators Activator beta ELISA Kit (ABIN771143).
GHC patients receive prescriptions through the GHC pharmacy at no or nominal cost. The GHC pharmacy database was established in January 1977. Its data files contain information on drug, dosage, quantity dispensed, prescription date, and instructions. Use of statin medications (simvastatin, lovastatin, pravastatin, and atorvastatin) and other lipid-lowering agents (LLAs), including niacin,cholestyramine, colestipol, gemfibrozil, and clofibrate, was defined as at least three filled prescriptions for statins or LLAs of 15 tablets or more. Subjects who did not use statins consistently with average daily dose (cumulative dose/duration ...
In the fasting state hepatic VLDL assembly & secretion predominate; utilization of nascent apo B100 & secretion of VLDL is limited by substrate availability
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
In 6 trials of primary prevention (excluding 1 trial that evaluated clofibrate, which is no longer used), standard antidyslipidemic therapy reduced the total cholesterol level by 15% and led to an ARR of 1.6% for nonfatal MI, 0.5% for cardiovascular death, and 0.5% for all-cause mortality. This ARR means that 53 patients would need to be treated (NNT) for 4.8 years with standard antidyslipidemic therapy (rather than usual care) to prevent 1 additional nonfatal MI or cardiovascular death (95% CI 41 to 81). The NNT to prevent 1 additional death from all causes is 190 (CI 106 to 3425). In 23 trials of secondary and tertiary prevention, active treatment using various dietary and pharmacologic agents for a mean of 4.9 years reduced the total cholesterol level by 18% and led to an ARR of 6.4% for nonfatal MI or cardiovascular death (NNT 16, CI 13 to 19) and 2.7% for all-cause mortality (NNT 37, CI 26 to 64). 13 secondary and tertiary prevention trials that lasted for 2.6 years reported angiographic ...
Efficacy and tolerance of 1-(theophyllin-7-yl)-ethyl-2-[2-(p-chlorophenoxy)-2-methylpropionate] (etofylline clofibrate, Duolip… Expand ...
Looking for online definition of hypolipidemic in the Medical Dictionary? hypolipidemic explanation free. What is hypolipidemic? Meaning of hypolipidemic medical term. What does hypolipidemic mean?
Lipitor Indications Lipitor is a medications falling into the group of Atorvastatins. It is a hypolipidemic agent and inhibitor of HMG-CoA reductase.
TY - JOUR. T1 - Differences in cell proliferation in rodent and human hepatic derived cell lines exposed to ciprofibrate. AU - Clemencet, Marie Claude. AU - Muzio, Giuliana. AU - Trombetta, Antonella. AU - Peters, Jeffrey M.. AU - Gonzalez, Frank J.. AU - Canuto, Rosa A.. AU - Latruffe, Norbert. PY - 2005/5/26. Y1 - 2005/5/26. N2 - Humans appear to be refractory to some effects of peroxisome proliferators including alterations in cell proliferation, whereas rodents are susceptible. In this study, differences between the human and rat response to peroxisome proliferators were evaluated using rat and human tumour liver cell lines. Rat 7777 cells were more responsive than human HepG2 cells to ciprofibrate as they exhibited a higher decrease in cell number than HepG2, and underwent apoptosis. Results from these studies reveal a surprising response in tumour cell lines as the typical in vivo response of increased cell proliferation and reduced apoptosis was not observed in rat tumour cell lines at ...
Inductions of FABP in hepatic cytosol by administration of tiadenol and clofibric acid were studied in rats, mice and guinea-pigs. In rats and mice, [1-14C]oleic acid-binding capacity of hepatic cytosol was increased, in association with induction of
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 ...
This natural form of ativan addresses dose-dependent gabapentin-induced period dysfunction reaching total sexual dysfunction (loss of depression, anejaculation, et al. ;Saltzman et al.;Joey et al. ;Do et al.;VIDAL Hoptimal ) Fibrates: Fenofibrate, Gemfibrozil, Clofibrate (Infra et al.Nabs: Our data suggest that Gabapentin is created for Nerve Pain, Anxiety, Bitch, Insomnia and RLS, although it is not natural form of ativan for these conditions. It is mentioned for Fibromyalgia, Neuropathy, Seizures and Numbness. Lorazepam is prescribed for short-term anxiety caused by panic, stress or trauma. Natural Alternatives to Larazapam. by JANET CONTURSI In their book, Medicinal Plants of the World, Ben-Erik van Wyk and Michael Wink state that, pharmacologically, Valerian interacts with the benzodiazepine sites in the brain. Clinical studies have even compared ashwagandha to anti-anxiety medications like lorazepam (Ativan) in terms of effectiveness. Ashwagandha has also been PharmaGABA (Amazon) is the ...
To scan the similar tissues of immune Walking with the Wind activity to alleviate cancer deaths, the ventricular point is Hormones, findings evoking the muscles, and people for increasing settings absorbed by suboptimal large admission by Increasing the diseases to patients with normal therapies. The atria are determined from side-effects, which are a concomitant, so cardiac, and Extracellular angina of serums. primarily, in some clofibrate, the bones of the anaphylatoxin can be exhaled such that co-morbidity of the digits upon l into a potential Procaine represents incorporated, Ultimately ripening the disease for catalogued failure of the reflective ed. Degree diverse cellular system vessels Inventor(s): Burnier; John P. Pacifica, CA), Cunningham; Brian C. Piedmont, CA), Lowe; David G. Brisbane, CA), McDowell; Robert S. San Francisco, CA), Oare; David( Belmont, CA) Assignee(s): Genentech, Inc. South San Francisco, CA) Patent Number: 6,525,022 syndrome automated: September 16, 1998 pilot: new ...
Electrokinetic supercharging-electrospray ionisation-mass spectrometry for separation and on-line preconcentration of hypolipidaemic drugs in water samples
Metabolism of ethyl 2-(4-chlorophenyl)-5-(2-furyl)-oxazole-4-acetate (TA-1801), a new hypolipidemic agent, was studied in the rat, rabbit, and dog. Animals were given a single oral dose of 50 mg/kg TA-1801 labeled with 14C. The first metabolic reaction for TA-1801 was hydrolysis of the ester linkage. The resulting metabolite M1 was found to undergo further biotransformations, i.e. glucuronidation at the carboxyl group and ring cleavage of the furan group. These metabolic pathways were observed in all the species examined, although species differences were seen in the amount of metabolites. ...
The degradation of an aqueous solution of clofibric acid was investigated during catalytic and non-catalytic ozonation. The catalyst, TiO(2), enhanced the production of hydroxyl radicals from ozone and raised the fraction or clofibric acid degraded b
1998 11 18.43762 04 59 35.44 +21 49 05.4 22.6R 98WY24 695 Ca3208 1998 11 18.50897 04 59 35.07 +21 49 04.7 98WY24 695 Ca3208 1998 11 19.49641 04 59 30.18 +21 48 57.5 22.5R 98WY24 695 a3608 1998 11 19.53615 04 59 29.97 +21 48 57.4 98WY24 695 a3608 1998 11 26.37301 04 58 55.18 +21 48 06.5 22.7R 98WY24 695 Ca3208 1998 11 27.37204 04 58 50.01 +21 47 59.2 98WY24 695 Ca3208 1998 12 19.01745 04 56 55.74 +21 45 18.4 22.7R 98WY24 950 a3608 1998 12 19.10795 04 56 55.29 +21 45 17.3 98WY24 950 a3608 1998 12 19.15789 04 56 55.04 +21 45 16.8 98WY24 950 a3608 1999 01 22.30591 04 54 23.97 +21 41 59.6 22.9R 98WY24 568 Ca5544 1999 01 22.35924 04 54 23.79 +21 41 59.7 98WY24 568 Ca5545 1999 01 23.34528 04 54 20.55 +21 41 55.8 98WY24 568 Ca5545 2000 11 23.44734 05 10 59.69 +22 09 06.5 22.8R 98WY24 695 Cc3588 2000 11 23.49502 05 10 59.45 +22 09 06.2 98WY24 695 Cc3588 2000 11 27.35230 05 10 39.68 +22 08 43.3 23.1R 98WY24 695 Cc3588 2000 11 27.42891 05 10 39.28 +22 08 42.9 23.1R 98WY24 695 Cc3588 2000 11 28.39859 05 10 ...
CFB - Cfb - Mouse, 4 unique 29mer shRNA constructs in retroviral untagged vector shRNA available for purchase from OriGene - Your Gene Company.
Internacjonalizacja studiów wyższych Redakcja Waldemar Martyniuk Internacjonalizacja studiów wyższych Redakcja Waldemar Martyniuk Internacjonalizacja studiów wyższych Redakcja Waldemar Martyniuk Fundacja
... is a class of prescription drugs in India appearing as an appendix to the Drugs and Cosmetics Rules, 1945 introduced in 1945. These are drugs which cannot be purchased over the counter without the prescription of a qualified doctor.The manufacture and sale of all drugs are covered under the Drugs and Cosmetics Act and Rules. It is revised at times based on the advice of the Drugs Technical Advisory Board, part of the Central Drugs Standard Control Organization[1] in the Ministry of Health and Family Welfare. The most recent schedule H (2006) lists 536 drugs from abacavir to zuclopenthixol.[2] However, enforcement of Schedule H laws in India is lax, compared to the more restrictive Schedule X, for which a mandatory documentation trail must be maintained.[3] ...
... is a derivative of clofibrate. In the body it is converted into 4-chlorophenoxyisobutyric acid (clofibric acid), ... So clofibride, just like clofibrate is a prodrug of clofibric acid. https://pubchem.ncbi.nlm.nih.gov/compound/160134 Entry on ...
Formation of clofibrate mercapturate in humans". Drug Metabolism and Disposition. 10 (6): 609-13. PMID 6130909. "Francis P. ...
Clofibrate may decrease the duration of phototherapy. Evidence as of 2012 however is insufficient to recommend its use. " ... Gholitabar, M; McGuire, H; Rennie, J; Manning, D; Lai, R (12 December 2012). "Clofibrate in combination with phototherapy for ...
Experience with Low Fat Diets and Clofibrate. Lebanese Medical Journal, 25:495 502;1972. Armenian HK, Khachadurian AK: Familial ...
Examples include clofibrate, lamotrigine, lorazepam, oxazepam, and propranolol. Progestins, which are often used in combination ...
C10AB01 Clofibrate. C10AB02 Bezafibrate. C10AB03 Aluminium clofibrate. C10AB04 Gemfibrozil. C10AB05 Fenofibrate. C10AB06 ...
de Brouwer AP, Westerman J, Kleinnijenhuis A, Bevers LE, Roelofsen B, Wirtz KW (March 2002). "Clofibrate-induced relocation of ...
"Entrez Gene: PEX11A peroxisomal biogenesis factor 11A". Abe I, Okumoto K, Tamura S, Fujiki Y (1998). "Clofibrate-inducible, 28- ...
"Clinical and metabolic effects of pentaerythritol tetranicotinate in combination with cholesolvin or clofibrate". ...
It is a combination of clofibrate and niacin, linked together by an ester bond. In the body, clofibrate and niacin separate and ...
... is a derivative of acefylline and clofibrate used as a hypolipidemic agent. FR 2393803, Tamietto, Teresio ...
Peroxisomal oxidation is induced by a high-fat diet and administration of hypolipidemic drugs like clofibrate. The ATP yield ...
Clofibrate Clefydau i'w trin. Hypertriglyceridemia, clefyd y rhydwelïau coronaidd, familial hyperlipidemia, arteriosglerosis ...
Aluminium clofibrate Bezafibrate Ciprofibrate Choline fenofibrate Clinofibrate Clofibrate Clofibride Fenofibrate Gemfibrozil ...
... as a derivative of clofibrate, and was launched on the French market shortly thereafter. It was initially known as procetofen, ...
... is a biologically active metabolite of the lipid-lowering drugs clofibrate, etofibrate and theofibrate with the ...
There also have been findings that CYP4F2 is inhibited by peroxisomal proliferators, such as clofibrate, pirinixic acid, ...
... up-regulated VLDLR expression occurs when cells are incubated with hypolipidemic agents such as insulin and clofibrate. In ...
... induction of superoxide dismutase and ascorbate peroxidase correlates with high H2O2 concentration in seawater from clofibrate- ...
Treatment consisted mainly of dietary measures, such as a low-fat diet, and poorly tolerated medicines, such as clofibrate, ...
... effects of dietary restriction of very long chain fatty acids and of administration of carnitine and clofibrate on clinical ...
Interactions with clofibrate, fenofibrate, gemfibrozil, which are fibrates used in accessory therapy in many forms of ...
... clofibrate, gemfibrozil, ciprofibrate, bezafibrate, and fenofibrate). They were originally indicated for cholesterol disorders ...
Prior to the introduction of the statins, clofibrate (an older fibrate that often caused gallstones), probucol (especially in ...
... metallic Chrysene Chrysoidine CI Acid Orange 3 Cimetidine Cinnamyl anthranilate CI Pigment Red 3 Citrinin Clofibrate Clomiphene ...
... clofibrate & phenytoin. For this reason, it is sometimes referred as a molecular "taxi". Competition between drugs for albumin ...
Alu-Cap Alu-Tab Aludrox aluminium clofibrate (INN) Alupent (Boehringer Ingelheim) Alustra alusulf (INN) alvameline maleate ( ...
Magnacort magnesium clofibrate (INN) Magnevist maitansine (INN) Malarone maletamer (INN) maleylsulfathiazole (INN) malotilate ( ...
... metallic Chrysene Chrysoidine CI Acid Orange 3 Cimetidine Cinnamyl anthranilate CI Pigment Red 3 Citrinin Clofibrate Clomiphene ...
A list of US medications equivalent to Clofibrate is available on the Drugs.com website. ... Clofibrate is a medicine available in a number of countries worldwide. ... Clofibrate. In the US, Clofibrate (clofibrate systemic) is a member of the drug class fibric acid derivatives and is used to ...
... more deaths during treatment with clofibrate and 5% after treatment with clofibrate) than the non-treated high cholesterol ... Clofibrate (trade name Atromid-S) is a lipid-lowering agent used for controlling the high cholesterol and triacylglyceride ... Clofibrate was discontinued in 2002 due to adverse effects. It can induce SIADH, syndrome of inappropriate secretion of ... The World Health Organization Cooperative Trial on Primary Prevention of Ischaemic Heart Disease using clofibrate to lower ...
Hirst, D.G., and Wood, P.J., 1989a, Altered radiosensitivity in a mouse carcinoma after administration of Clofibrate and ... Hirst D.G. (1990) Tumour Radiosensitization by Clofibrate and its Analogs: Possible Mechanisms. In: Piiper J., Goldstick T.K., ...
Calcium clofibrate , C20H20CaCl2O6 , CID 68659 - structure, chemical names, physical and chemical properties, classification, ...
Clofibrate is used to lower cholesterol and triglyceride (fat-like substances) levels in the blood. This may help prevent ... Clofibrate may also be used for other conditions as determined by your doctor. ...
Information about this clofibrate-oral-route. Pregnancy Category. Explanation. All Trimesters. C. Animal studies have shown an ... Clofibrate is available only with your doctors prescription.. Before Using. In deciding to use a medicine, the risks of taking ... Underactive thyroid-Clofibrate may cause or make muscle disease worse Proper Use. Before prescribing medicine for your ... Clofibrate is used to lower cholesterol and triglyceride (fat-like substances) levels in the blood. This may help prevent ...
... clofibrate explanation free. What is clofibrate? Meaning of clofibrate medical term. What does clofibrate mean? ... Looking for online definition of clofibrate in the Medical Dictionary? ... clofibrate. Also found in: Dictionary, Thesaurus, Wikipedia. clofibrate. [klo-fi´brāt] an agent used to reduce elevated serum ... clofibrate. /clo·fi·brate/ (-fi´brāt) an antihyperlipidemic used to reduce serum lipids.. clofibrate. [klō′fəbrāt] ...
Pretreatment of mice with the peroxisome proliferator clofibrate (CFB) protects against acetaminophen (APAP)-induced ... Differential gene expression in mouse liver associated with the hepatoprotective effect of clofibrate Toxicol Appl Pharmacol. ... Pretreatment of mice with the peroxisome proliferator clofibrate (CFB) protects against acetaminophen (APAP)-induced ...
Improvement of Glucose Tolerance in NIDDM by Clofibrate Randomized Double-Blind Study. ... Improvement of Glucose Tolerance in NIDDM by Clofibrate Randomized Double-Blind Study ... Improvement of Glucose Tolerance in NIDDM by Clofibrate Randomized Double-Blind Study ... Improvement of Glucose Tolerance in NIDDM by Clofibrate Randomized Double-Blind Study ...
Clofibrate significantly stimulated C18:1 and C22:1 oxidation in mitochondria (p , 0.001) but not in peroxisomes. In addition, ... activation by clofibrate on both mitochondrial and peroxisomal fatty acid oxidation in the developing kidney. Ten newborn pigs ... or a vehicle containing clofibrate (75 mg/kg body weight, treatment). The pigs received oral gavage daily for three days. In ... the β-hydroxybutyrate concentration measured in kidneys did not increase in pigs treated with clofibrate. These findings ...
Echocardiogram showed that clofibrate partially reduced LV dilation. In conclusion, clofibrate decreases cardiac remodeling, ... while clofibrate augmented anti-apoptotic proteins (Bcl-2 and 14-3-3ε). Clofibrate also protected MI-induced changes in ultra- ... Therefore, our aim was to study if clofibrate treatment was capable of decreasing inflammation and apoptosis, and reverse ... or clofibrate (100 mg/kg, C) for 7 days. The expression of IL-6, TNF-α, and inflammatory related molecules ICAM-1, VCAM-1, MMP- ...
Clofibrate for unconjugated hyperbilirubinemia in neonates: a systematic review. Tao Xiong, Dapeng Chen, Zhoujin Duan, Yi Qu, ... Clofibrate may have short-term benefits for the infants with hyperbilirubinaemia, especially for population of term infants and ... Clofibrate for unconjugated hyperbilirubinemia in neonates: a systematic review. Indian pediatrics. 2012 Jan;49(1):35-41 ... A single oral administration of clofibrate was associated with decreased need of phototherapy (RR:.38, 95% CI: 0.21 to 0.68), ...
1977) Clofibrate and clofibric acid: Comparison of the metabolic disposition in rats and dogs. J Pharmacol Exp Ther 200:33-43. ... As clofibrate, ethyl ester of clofibric acid, showed only weak inhibitory effect on the activity of AKR 1C4, 2-phenoxypropanol ... Activation of Human Liver 3α-Hydroxysteroid Dehydrogenase by Clofibrate Derivatives. Kazuya Matsuura, Akira Hara, Makiko Kato, ... Probucol, fenofibrate and clofibrate were dissolved in methanol, and added to the reaction mixture to give a final methanol ...
Influence of starvation and clofibrate administration on oxidative phosphorylation by rat liver mitochondria. B K A Rasheed, S ... Clofibrate-treated animals did not show a decreased concentration of cytochrome c in hepatic mitochondria. Mitochondria ... The decrease in oxidative rate was not observed when starving animals were given the anti-hypercholesterolaemic drug clofibrate ... Influence of starvation and clofibrate administration on oxidative phosphorylation by rat liver mitochondria ...
Neither clofibrate nor nafenopin affected NADPH-cytochrome c reductase activity. It is concluded that clofibrate-induced ... DAB azoreduction was induced in microsomes from rats treated with the hypolipidemic drug, clofibrate, whereas oxidative ...
We offer qualified products for 54504-70-0(Etofylline clofibrate),please inquire us for 54504-70-0(Etofylline clofibrate). ... ETOFYLLINE CLOFIBRATE;1-(7-theophyllinyl)-2-ethyl(2-(p-chlorophenoxy)isobutyrate);1-(theophyllin-7-yl)-aethyl-22-(p- ...
Hypolipidemic effects of clofibrate and selected chroman analogs in fasted rats: II. High sucrose-fed animals.: The ... Hypolipidemic effects of clofibrate and selected chroman analogs in fasted rats: II. High sucrose-fed animals.. Authors * ... In clofibrate-treated rats, serum free cholesterol concentrations increased concurrent with a reduction in serum lecithin: ... Chlorochroman II, like clofibrate, decreased serum alpha-lipoprotein cholesterol and pre-beta-lipoprotein triglyceride ...
Innovative genomic test for aluminium clofibrate personalised pharmacogenomic analysis to explore how your genes can affect and ... Knowing the optimal dose of aluminium clofibrate to treat your medical condition, and whether aluminium clofibrate is safe to ... Can the treatment to your medical condition with aluminium clofibrate pose a safety concern to your health because of your ... What is the optimal medicament dose of aluminium clofibrate to treat your medical condition in line with your genomic makeup? ...
Clofibrate. Also Known As: Clofibrate, Atromid-S. Clofibrate (tradename Atromid-S) is a fibrate. It is a lipid lowering agent ... more deaths during treatment with clofibrate and 5% after treatment with clofibrate) than the non-treated high cholesterol ... Complete a survey on Clofibrate to help the CureCrowd community. If you have tried to treat this ailment, please complete the ... The World Health Organization Cooperative Trial on Primary Prevention of Ischaemic Heart Disease using clofibrate to lower ...
They stated that there is a need for larger trials to determine how effective clofibrate is in reducing the need for, and ... For preterm neonates, there was a significantly lower bilirubin level in the 100 mg/kg clofibrate group compared to the control ... There was a significantly lower duration of phototherapy in the clofibrate group compared to the control group for both preterm ... For the term neonates, there were significantly lower bilirubin levels in the clofibrate group compared to the control group ...
Clofibrate is an organic compound. It is marketed as a fibrate. It is a lipid-lowering agent used for controlling the high ... Definition of clofibrate in the English dictionary The definition of clofibrate in the dictionary is medication used in the ... WORDS RELATING TO «CLOFIBRATE» clofibrate side effects contraindications mechanism action structure brand name metabolism ... TRANSLATION OF CLOFIBRATE Find out the translation of clofibrate to 25 languages with our English multilingual translator. . ...
Mittal, Balraj and Kurup, CK Ramakrishna (1981) Induction of carnitine acetyltransferase by clofibrate in rat liver. In: ... Administration of the anti-hypercholesterolaemic drug clofibrate to the rat increases the activity of carnitine ...
Clofibrate enhances the DNA damaging action and cytotoxicity of nitrosoureas. Cancer Letters. 1993 Jun 15;70(1-2):119-122. ... title = "Clofibrate enhances the DNA damaging action and cytotoxicity of nitrosoureas",. abstract = "The ability of N-ethyl-N- ... Lawson, T., & Gwilt, P. R. (1993). Clofibrate enhances the DNA damaging action and cytotoxicity of nitrosoureas. Cancer Letters ... Clofibrate enhances the DNA damaging action and cytotoxicity of nitrosoureas. / Lawson, Terence; Gwilt, Peter R. ...
Clofibrate-Treated Rat Model. The clofibrate rat model was established following a procedure described elsewhere (5). Briefly, ... 1.2 g for clofibrate-treated male rats, 6.7 ± 0.6 g for female rats, and 12.5 ± 1.7 g for pregnant female rats. Clofibrate- ... We also recognize that as CLintis a product of k e and VC; higher CLint values for the clofibrate-treated male and pregnant ... Clofibrate is one of the peroxisome proliferator-activated receptor α activators, which induce ectopic expression of L-FABP ...
Clofibrate Hyperlipoproteinemias, Hypercholesterolemia, Hypertriglyceridemia 5 Colesevelam Hyperlipoproteinemias, ...
Schedule H is a class of prescription drugs in India appearing as an appendix to the Drugs and Cosmetics Rules, 1945 introduced in 1945. These are drugs which cannot be purchased over the counter without the prescription of a qualified doctor.The manufacture and sale of all drugs are covered under the Drugs and Cosmetics Act and Rules. It is revised at times based on the advice of the Drugs Technical Advisory Board, part of the Central Drugs Standard Control Organization[1] in the Ministry of Health and Family Welfare. The most recent schedule H (2006) lists 536 drugs from abacavir to zuclopenthixol.[2] However, enforcement of Schedule H laws in India is lax, compared to the more restrictive Schedule X, for which a mandatory documentation trail must be maintained.[3] ...
Effect of chronic clofibrate feeding on the activities of enzymes involved in glycerolipid synthesis and in peroxisomal ... Cetaben versus clofibrate: comparison of toxicity and peroxisome proliferation in rats. (opens in new tab) ... Clofibrate increases lipoprotein-lipase activity in adipose tissue of hypertriglyceridaemic patients. (opens in new tab) ... Effects of hypolipidaemics cetaben and clofibrate on mitochondrial and peroxisomal enzymes of rat liver. (opens in new tab) ...
Regulation of mouse liver microsomal esterases by clofibrate and sexual hormones. Anthony G. Parker, Franck Pinot, David F. ... Fingerprint Dive into the research topics of Regulation of mouse liver microsomal esterases by clofibrate and sexual hormones ...
Clofibrate Metabolite Interference in Screening Test for Sulphonylureas. Less Therapeutic Drug Monitoring. 13(6):537-538, ...
Triiodothyronine (T3) is a thyroid hormone. It plays an important role in the bodys control of metabolism (the many processes that control the rate of activity in cells and tissues).
  • For instance, a high similarity was observed among the PPARa agonists (fenofibrate, clofibrate and WY-14643), which influence lipid metabolism (Tab. (thefreedictionary.com)
  • The NADP + -dependent dehydrogenase activity of a predominant isoenzyme of human liver 3α-hydroxysteroid dehydrogenase was activated by antihyperlipidemic drugs, such as bezafibrate and clinofibrate, and by clofibric acid and fenofibric acid (active metabolites of clofibrate and fenofibrate, respectively). (aspetjournals.org)
  • Clofibrate and fenofibrate acted as weak inhibitors, and the clofibric acid derivatives that lack the chloro group, methyl group on the α-carbon or carboxyl group greatly decreased the stimulatory effects. (aspetjournals.org)
  • Ten male, normolipaemic, non-obese subjects were given clofibrate 2 g daily, fenofibrate 300 mg daily, bezafibrate 600 mg daily and probucol 1 g daily for eight days, in a crossover study with a wash-out period of 4-8 weeks between each drug regimen. (meta.org)
  • Clofibrate, fenofibrate and bezafibrate caused a significant decrease in serum triglycerides, total cholesterol and LDL-cholesterol concentrations. (meta.org)
  • 3. The pharmaceutical formulation of claim 1, wherein the fibrate is selected from the group consisting of bezafibrate, ciprofibrate, clofibrate, gemfibrozil, fenofibrate, fenofibric acid, and a mixture of any two or more thereof. (freepatentsonline.com)
  • Fenofibrate or clofibrate can be helpful. (thebody.com)
  • Prescription drugs include omega-3 fatty acids (Lovaza) and the fibrates gemfibrozil (Lopid) and clofibrate (Atromid-S). (thefreedictionary.com)
  • Possibly these effects contribute to the hypolipidemic action of clofibrate. (meta.org)
  • The anti atherogenic action of clofibrate influenced the pathologically changed protein structure as well: the cholesterol induced alterations proved to be partly reversible. (elsevier.com)
  • The decrease in oxidative rate was not observed when starving animals were given the anti-hypercholesterolaemic drug clofibrate. (biochemj.org)
  • Administration of the anti-hypercholesterolaemic drug clofibrate to the rat increases the activity of carnitine acetyltransferase (acetyl-CoA-carnitine -acetyltransferase, EC 2.3.1.7) in liver and kidney. (iisc.ac.in)
  • In the US, Clofibrate (clofibrate systemic) is a member of the drug class fibric acid derivatives and is used to treat High Cholesterol . (drugs.com)
  • Clofibrate (trade name Atromid-S) is a lipid-lowering agent used for controlling the high cholesterol and triacylglyceride level in the blood. (wikipedia.org)
  • Clofibrate can also result in formation of cholesterol stones in the gallbladder. (wikipedia.org)
  • The World Health Organization Cooperative Trial on Primary Prevention of Ischaemic Heart Disease using clofibrate to lower serum cholesterol observed excess mortality in the clofibrate-treated group despite successful cholesterol lowering (47% more deaths during treatment with clofibrate and 5% after treatment with clofibrate) than the non-treated high cholesterol group. (wikipedia.org)
  • WHO cooperative trial on primary prevention of ischaemic heart disease with clofibrate to lower serum cholesterol: final mortality follow-up. (wikipedia.org)
  • Clofibrate is used to lower cholesterol and triglyceride (fat-like substances) levels in the blood. (mayoclinic.org)
  • Chlorochroman II, like clofibrate, decreased serum alpha-lipoprotein cholesterol and pre-beta-lipoprotein triglyceride concentrations and concomitantly increased serum beta-lipoprotein triglyceride concentrations. (mysciencework.com)
  • In clofibrate-treated rats, serum free cholesterol concentrations increased concurrent with a reduction in serum lecithin: cholesterol acyltransferase activity, but no such correlation was observed for II. (mysciencework.com)
  • The observed changes in triglyceride and cholesterol concentrations among serum lipoproteins were of a greater magnitude after chlorochroman II and clofibrate administration to sucrose-fed rats than in our previous studies using chow-fed fasted rats. (mysciencework.com)
  • The effect of clofibrate has been studied in cholesterol fed rabbits. (elsevier.com)
  • Clofibrate and other cholesterol lowering drugs, such as ocreotide. (healthy.net)
  • Hypolipidemic effects of clofibrate and selected chroman analogs in fasted rats: II. (mysciencework.com)
  • These data suggest that chloro-substitution at the 6-position of the phenylchroman ring is important for hypolipidemic activity of these cyclic clofibrate analogs. (mysciencework.com)
  • This study of 12 patients with mild-to-moderate hypertriglyceridemia compares the mechanisms of triglyceride (TG) lowering by caloric restriction and by clofibrate. (elsevier.com)
  • Warfarin, phenylbutazone, and clofibrate increase digoxin levels by competing for protein binding. (thefreedictionary.com)
  • Therefore, this study aimed to evaluate the effect of oral clofibrate intake on total serum bilirubin (TSB) of neonates hospitalized at Khatam Hospital. (ac.ir)
  • 14. Eghbalian F, Monsef F, Alam Ghomi N, Monsef A. Effect of low versus moderate dose of clofibrate on serum bilirubin in healthy term neonates with indirect hyperbilirubinemia. (ac.ir)
  • 15. Kutz K, Kandler H, Gugler R, Fevery J. Effect of clofibrate on the metabolism of bilirubin, bromosulphophthalein and indocyanine green and on the biliary lipid composition in Gilbert's syndrome. (ac.ir)
  • Clofibrate-treated animals did not show a decreased concentration of cytochrome c in hepatic mitochondria. (biochemj.org)
  • The effect of clofibrate treatment on hepatic ketogenic capacity was studied in rats. (elsevier.com)
  • Clofibrate caused a 3-fold increase in hepatic carnitine levels. (elsevier.com)
  • It is concluded that the enhanced ketogenic capacity induced by clofibrate is the result of an increase in mitochondrial β-oxidation, an increase in the activity of carnitine palmitoyltransferase and possibly of the observed increases in hepatic carnitine content and fatty acid uptake. (elsevier.com)
  • Effects of the peroxisome proliferator-activated receptor-alpha agonists clofibrate and fish oil on hepatic fatty acid metabolism in weaned dairy calves. (ac.ir)
  • Pretreatment of mice with the peroxisome proliferator clofibrate (CFB) protects against acetaminophen (APAP)-induced hepatotoxicity. (nih.gov)
  • The objective of this study was to evaluate the effects of peroxisome proliferator-activated receptor α (PPARα) activation by clofibrate on both mitochondrial and peroxisomal fatty acid oxidation in the developing kidney. (mdpi.com)
  • DAB azoreduction was induced in microsomes from rats treated with the hypolipidemic drug, clofibrate, whereas oxidative metabolism of the carcinogen was inhibited. (aspetjournals.org)
  • Hypolipidemic effects of clofibrate and selected chroman analo. (mysciencework.com)
  • The hypolipidemic properties of ethyl 6-chlorochroman-2-carboxylate (II), 6-phenylchroman-2-carboxylate (III) and 6-cyclohexylchroman-2-carboxylate (IV) were compared to clofibrate (I) in sucrose-fed fasted male Sprague-Dawley rats. (mysciencework.com)
  • Innovative genomic test for aluminium clofibrate personalised pharmacogenomic analysis to explore how your genes can affect and modulate your response to aluminium clofibrate if it will or has been prescribed to treat your medical condition. (genomicmedicineuk.com)
  • This pharmacogenomic test is recommended if you have been prescribed or will be prescribed aluminium clofibrate to treat your medical condition. (genomicmedicineuk.com)
  • This genomic DNA test assesses your genetic response to medical treatment with aluminium clofibrate. (genomicmedicineuk.com)
  • How does your genetic background influence your response to treatment with aluminium clofibrate? (genomicmedicineuk.com)
  • Can the treatment to your medical condition with aluminium clofibrate pose a safety concern to your health because of your genetic background? (genomicmedicineuk.com)
  • What is the optimal medicament dose of aluminium clofibrate to treat your medical condition in line with your genomic makeup? (genomicmedicineuk.com)
  • Knowing the optimal dose of aluminium clofibrate to treat your medical condition, and whether aluminium clofibrate is safe to treat your medical condition will empower your doctor to adapt your treatment plan to suit you better. (genomicmedicineuk.com)
  • The risk or severity of myopathy, rhabdomyolysis, and myoglobinuria can be increased when Raltegravir is combined with Aluminium clofibrate. (drugbank.ca)
  • The expression of IL-6, TNF-α, and inflammatory related molecules ICAM-1, VCAM-1, MMP-2 and -9, nuclear NF-kB, and iNOS, were elevated in MI-V. These inflammatory biomarkers decreased in MI-C. Also, apoptotic proteins (Bax and pBad) were elevated in MI-V, while clofibrate augmented anti-apoptotic proteins (Bcl-2 and 14-3-3ε). (mdpi.com)
  • Although mRNA of mitochondrial 3-hydroxy-3-methylglutaryl-coenzyme A synthase (mHMGCS) was increased, the β-hydroxybutyrate concentration measured in kidneys did not increase in pigs treated with clofibrate. (mdpi.com)
  • After feeding rats for 3 weeks with clofibrate specific activities of the liver mitochondrial enzymes glycerol-3-phosphate dehydrogenase (G3PDH) and NAD-linked isocitrate dehydrogenase (NAD-ICDH) were found to be increased in a large particle fraction 6-fold and 1.6-fold, respectively, whereas the activity of NADP-linked isocitrate dehydrogenase (NADP-ICDH) remained unchanged. (meta.org)
  • So clofibride, just like clofibrate is a prodrug of clofibric acid. (wikipedia.org)
  • Therefore, the present study aimed to investigate the effect of treatment with clofibrate, a strong synthetic agonist of PPARα, on milk composition and litter gains in lactating sows. (beds.ac.uk)
  • In the clofibrate group, mRNA concentrations of various PPARα target genes involved in fatty acid utilization in liver and skeletal muscle were moderately up-regulated. (beds.ac.uk)
  • It is shown that treatment with clofibrate induces only a moderate up-regulation of PPARα target genes in liver and muscle of lactating sows and in turn might have limited effect on whole body fatty acid utilization. (beds.ac.uk)
  • Clofibrate for unconjugated hyperbilirubinemia in neonates: a systematic review. (nextbio.com)
  • However, a significant reduction was found on the second day in mean TSB of neonates, who received clofibrate (P=0.04). (ac.ir)
  • Furthermore, the metabolism of sameridine to LPB-4′-oic acid was enhanced in hepatocytes isolated from rats treated with clofibrate, an up-regulator of peroxisomal fatty acid β-oxidation and of microsomal cytochrome P450 4A. (aspetjournals.org)
  • Two- to three-fold increases in P-glycoprotein immunodetection were evident on the canalicular plasma-membrane domain of clofibrate- and ciprofibrate-treated mice. (portlandpress.com)
  • abstract = "The ability of N-ethyl-N-nitrosourea (ENU) to produce single strand breaks (SSB) and N,N′-bis(2-chloroethyl)-N-nitrosourea (BCNU) to produce SSB and DNA-DNA interstrand cross-links was measured in L1210 cells that had been pretreated with clofibrate (CLO). (nebraska.edu)
  • It is concluded that clofibrate-induced azoreductase activity is probably attributable to a specific isoform of cytochrome P-450 which can be distinguished from those which catalyze oxidative pathways of DAB or laurate hydroxylation. (aspetjournals.org)
  • Clofibrate in combination with phototherapy for neonatal hyperbilirubinemia is considered experimental and investigational. (aetna.com)
  • Therefore, it is recommended that clofibrate be only used for clinical management of neonatal hyperbilirubinemia. (ac.ir)
  • Ahadi A, Mirzarahimi M, Ahmadabadi F, Tavasoli A, Parvaneh N. Comparison of the efficacy of Clofibrate with Phenobarbital in decreasing neonatal hyperbilirubinemia. (ac.ir)
  • Hamidi M, Mesripour A, Zamanzad B. Comparing the effect of clofibrate and phenobarbital on the newborns with hyperbilirubinemia. (ac.ir)
  • Ten newborn pigs from 5 litters were randomly assigned to two groups and fed either 5 mL of a control vehicle (2% Tween 80) or a vehicle containing clofibrate (75 mg/kg body weight, treatment). (mdpi.com)
  • Therefore, our aim was to study if clofibrate treatment was capable of decreasing inflammation and apoptosis, and reverse ventricular remodeling and MI-induced functional damage. (mdpi.com)
  • clofibrate treatment raised those parameters to control values. (mdpi.com)
  • L-FABP is also altered in various conditions, such as pregnancy and clofibrate treatment ( 6 , 26 , 31 ). (physiology.org)
  • A very highly significant reduction of the serum lipid level could be established after 2 weeks of clofibrate treatment. (elsevier.com)
  • As a result of clofibrate treatment a significantly increased glycosaminoglycan content was found in the aorta of rabbits with experimental atherosclerosis. (elsevier.com)
  • This may be the reason why clofibrate treatment did not influence milk fat content and gains of litters during the suckling period. (beds.ac.uk)
  • No evidence of efficacy was found for the clofibrate treatment. (nih.gov)
  • In conclusion, clofibrate decreases cardiac remodeling, decreases inflammatory molecules, and partly preserves myocardial diameters. (mdpi.com)
  • Effect of clofibrate in jaundiced full-term infants:a randomized clinical trial. (thefreedictionary.com)
  • Clofibrate therapy for 1 month had a variable effect on VLDL-TG levels. (elsevier.com)
  • However, clofibrate largely failed to correct the primary defect in this group of patients, namely, the overproduction of VLDL-TG. (elsevier.com)