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.
Valerates are salts or esters formed from the reaction between valerianic acid and a base, characterized by their tranquilizing and sedative properties, often used in pharmaceuticals and dietary supplements for promoting sleep and reducing anxiety.
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.

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)

Clofibrate is a medication that belongs to the class of drugs known as fibrates. It is primarily used to lower elevated levels of cholesterol and other fats (lipids) in the blood, specifically low-density lipoprotein (LDL), or "bad" cholesterol, and triglycerides, while increasing high-density lipoprotein (HDL), or "good" cholesterol. Clofibrate works by reducing the production of very-low-density lipoproteins (VLDL) in the liver, which in turn lowers triglyceride levels and indirectly reduces LDL cholesterol levels.

Clofibrate is available in oral tablet form and is typically prescribed for patients with high cholesterol or triglycerides who are at risk of cardiovascular disease, such as those with a history of heart attacks, strokes, or peripheral artery disease. It is important to note that clofibrate should be used in conjunction with lifestyle modifications, including a healthy diet, regular exercise, and smoking cessation.

Like all medications, clofibrate can have side effects, some of which may be serious. Common side effects include stomach upset, diarrhea, gas, and changes in taste. Less commonly, clofibrate can cause more severe side effects such as liver or muscle damage, gallstones, and an increased risk of developing certain types of cancer. Patients taking clofibrate should be monitored regularly by their healthcare provider to ensure that the medication is working effectively and to monitor for any potential side effects.

Halofenate is not typically considered a medication with a primary use in modern medical practice. However, historically it has been used as a treatment for gout and hyperuricemia (high levels of uric acid in the blood). It is a compound with both uricosuric and anti-inflammatory properties.

The uricosuric action of halofenate helps to lower serum uric acid levels by increasing its excretion in the urine, while its anti-inflammatory effects may help alleviate symptoms associated with gout attacks. It is important to note that due to its limited use and potential side effects, other medications are often preferred for managing gout and hyperuricemia.

Please consult a healthcare professional or pharmacist for more information about specific medications and treatment options.

Hypolipidemic agents are a class of medications that are used to lower the levels of lipids (fats) in the blood, particularly cholesterol and triglycerides. These drugs work by reducing the production or increasing the breakdown of fats in the body, which can help prevent or treat conditions such as hyperlipidemia (high levels of fats in the blood), atherosclerosis (hardening and narrowing of the arteries), and cardiovascular disease.

There are several different types of hypolipidemic agents, including:

1. Statins: These drugs block the action of an enzyme called HMG-CoA reductase, which is necessary for the production of cholesterol in the liver. By reducing the amount of cholesterol produced, statins can help lower LDL (bad) cholesterol levels and increase HDL (good) cholesterol levels.
2. Bile acid sequestrants: These drugs bind to bile acids in the intestines and prevent them from being reabsorbed into the bloodstream. This causes the liver to produce more bile acids, which requires it to use up more cholesterol, thereby lowering LDL cholesterol levels.
3. Nicotinic acid: Also known as niacin, this drug can help lower LDL and VLDL (very low-density lipoprotein) cholesterol levels and increase HDL cholesterol levels. It works by reducing the production of fatty acids in the liver.
4. Fibrates: These drugs are used to treat high triglyceride levels. They work by increasing the breakdown of fats in the body and reducing the production of VLDL cholesterol in the liver.
5. PCSK9 inhibitors: These drugs block the action of a protein called PCSK9, which helps regulate the amount of LDL cholesterol in the blood. By blocking PCSK9, these drugs can help lower LDL cholesterol levels.

It's important to note that hypolipidemic agents should only be used under the guidance and supervision of a healthcare provider, as they can have side effects and may interact with other medications.

Alkane 1-monooxygenase is an enzyme that catalyzes the addition of one oxygen atom from molecular oxygen to a alkane, resulting in the formation of an alcohol. This reaction also requires the cofactor NADH or NADPH and generates water as a byproduct.

The general reaction catalyzed by alkane 1-monooxygenase can be represented as follows:

R-CH3 + O2 + NAD(P)H + H+ -> R-CH2OH + H2O + NAD(P)+

where R represents an alkyl group.

This enzyme is found in various microorganisms, such as bacteria and fungi, and plays a crucial role in their ability to degrade hydrocarbons, including alkanes, which are major components of fossil fuels. Alkane 1-monooxygenase has potential applications in bioremediation and the production of biofuels from renewable resources.

Microbodies are small, membrane-bound organelles found in the cells of eukaryotic organisms. They typically measure between 0.2 to 0.5 micrometers in diameter and play a crucial role in various metabolic processes, particularly in the detoxification of harmful substances and the synthesis of lipids.

There are several types of microbodies, including:

1. Peroxisomes: These are the most common type of microbody. They contain enzymes that help break down fatty acids and amino acids, producing hydrogen peroxide as a byproduct. Another set of enzymes within peroxisomes then converts the harmful hydrogen peroxide into water and oxygen, thus detoxifying the cell.
2. Glyoxysomes: These microbodies are primarily found in plants and some fungi. They contain enzymes involved in the glyoxylate cycle, a metabolic pathway that helps convert stored fats into carbohydrates during germination.
3. Microbody-like particles (MLPs): These are smaller organelles found in certain protists and algae. Their functions are not well understood but are believed to be involved in lipid metabolism.

It is important to note that microbodies do not have a uniform structure or function across all eukaryotic cells, and their specific roles can vary depending on the organism and cell type.

Peroxisome proliferators are a class of synthetic compounds that can induce the proliferation (i.e., increase in number) of peroxisomes in the cells of various organisms, including mammals. These compounds include certain pharmaceuticals, industrial chemicals, and environmental pollutants.

Peroxisomes are small, membrane-bound organelles found in the cytoplasm of eukaryotic cells (cells with a true nucleus). They play a crucial role in several metabolic processes, including the breakdown of fatty acids, the detoxification of harmful substances, and the biosynthesis of certain lipids.

Peroxisome proliferators exert their effects by binding to and activating specific nuclear receptors called peroxisome proliferator-activated receptors (PPARs). PPARs are transcription factors that regulate the expression of genes involved in cellular metabolism, differentiation, and growth. Activation of PPARs by peroxisome proliferators leads to an increase in peroxisome number and altered peroxisomal functions, which can have various consequences for cellular homeostasis and overall organism health.

It is important to note that long-term exposure to certain peroxisome proliferators has been linked to increased risks of cancer and other diseases in animals, although the evidence in humans is less clear. Further research is needed to fully understand the potential health impacts of these compounds.

Hypoglycin A and Hypoglycin B are two related compounds that are found in some plants, particularly in the unripe seeds and leaves of the African locust bean (Parkia speciosa) and the Caribbean shrub, bitter cassava (Manihot esculenta). These compounds are known to inhibit the enzyme called glutamic-oxaloacetic transaminase, which is important for amino acid metabolism.

Hypoglycin A is particularly toxic and can cause a condition known as hypoglycemia (low blood sugar) in both humans and animals. This occurs when the compound interferes with the body's ability to produce glucose, which is needed for energy production. In addition to hypoglycemia, Hypoglycin A can also cause other symptoms such as vomiting, weakness, and seizures.

Hypoglycin B is less toxic than Hypoglycin A but can still cause illness in some cases. It has been linked to a condition called "malignant catarrhal jaundice," which is a severe form of liver disease that can occur in people who consume large amounts of bitter cassava.

Both Hypoglycin A and B are heat-stable, which means that cooking or processing the plants that contain them does not reduce their toxicity. Therefore, it is important to avoid consuming these compounds in large quantities.

Gemfibrozil is a medication that belongs to a class of drugs called fibrates. It is primarily used to lower elevated levels of triglycerides (a type of fat found in the blood) and increase levels of "good" cholesterol (HDL-C) in the blood.

Gemfibrozil works by reducing the production of triglycerides in the body, increasing the breakdown of fats in the liver, and improving the way the body handles fats and sugar. It is often prescribed for people with high triglyceride levels who are at risk for pancreatitis (inflammation of the pancreas) or those who have not responded well to other cholesterol-lowering medications, such as statins.

It's important to note that while gemfibrozil can help manage triglyceride and cholesterol levels, it is not a substitute for a healthy lifestyle. Regular exercise, a balanced diet, limiting alcohol consumption, and avoiding smoking are all crucial components of maintaining good cardiovascular health.

As with any medication, gemfibrozil should be taken under the supervision of a healthcare provider, who can monitor its effectiveness and potential side effects. Common side effects of gemfibrozil include stomach pain, diarrhea, and muscle or joint pain. Rare but serious side effects may include liver damage, kidney problems, and an increased risk of gallstones.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Clofibric acid is the main metabolic product of clofibrate, a medication that belongs to the class of drugs called fibrates. It works by lowering levels of total and LDL (low-density lipoprotein) cholesterol and triglycerides in the blood, while increasing HDL (high-density lipoprotein) cholesterol levels. Clofibric acid is an antihyperlipidemic agent that is used primarily for the treatment of hypertriglyceridemia and mixed dyslipidemia. It may also be used to prevent pancreatitis caused by high triglyceride levels.

Clofibric acid is detectable in the urine and can be used as a biomarker for clofibrate exposure or use. However, it's important to note that clofibrate has largely been replaced by newer fibrates and statins due to its adverse effects profile and lower efficacy compared to these newer agents.

Fibric acids, also known as fibric acid derivatives, are a class of medications that are primarily used to lower elevated levels of triglycerides (a type of fat) in the blood. They work by increasing the breakdown and removal of triglycerides from the bloodstream, and reducing the production of very-low-density lipoprotein (VLDL), a type of particle that carries triglycerides in the blood.

Examples of fibric acids include gemfibrozil, fenofibrate, and clofibrate. These medications are often prescribed for people with high triglyceride levels who are at risk for pancreatitis (inflammation of the pancreas) or other complications related to high triglycerides.

Fibric acids may also have a modest effect on raising levels of high-density lipoprotein (HDL), or "good" cholesterol, and lowering levels of low-density lipoprotein (LDL), or "bad" cholesterol, in some people. However, they are generally not as effective at lowering LDL cholesterol as statins, another class of cholesterol-lowering medications.

It's important to note that fibric acids can interact with other medications and may cause side effects such as stomach upset, muscle pain, and an increased risk of gallstones. As with any medication, it's important to use fibric acids under the guidance of a healthcare provider.

Clofenapate is a medication that was previously used as an anti-inflammatory drug, primarily for the treatment of rheumatoid arthritis and osteoarthritis. It belongs to a class of drugs known as fenamic acids or fenamates. Clofenapate works by reducing the production of prostaglandins, which are hormone-like substances that cause pain and inflammation in the body.

However, due to its potential for serious side effects, particularly on the heart, clofenapate is no longer widely used or available in many countries. It can have adverse cardiovascular effects such as increasing the risk of irregular heart rhythms, and it has been associated with severe liver toxicity in some cases. Therefore, its use is generally discouraged, and other safer and more effective treatment options are recommended for managing inflammatory conditions.

2-Methyl-4-chlorophenoxyacetic acid is a synthetic auxin, which is a type of plant hormone. It is often used as a herbicide to control broadleaf weeds in crops such as corn and wheat. It works by causing uncontrolled growth in the targeted plants, ultimately leading to their death. It is important to note that this compound is not typically used in human medicine.

Carnitine O-acetyltransferase (COAT) is an enzyme that plays a crucial role in the transport and metabolism of fatty acids within cells. It is also known as carnitine palmitoyltransferase I (CPT I).

The primary function of COAT is to catalyze the transfer of an acetyl group from acetyl-CoA to carnitine, forming acetylcarnitine and free CoA. This reaction is essential for the entry of long-chain fatty acids into the mitochondrial matrix, where they undergo beta-oxidation to produce energy in the form of ATP.

COAT is located on the outer membrane of the mitochondria and functions as a rate-limiting enzyme in fatty acid oxidation. Its activity can be inhibited by malonyl-CoA, which is an intermediate in fatty acid synthesis. This inhibition helps regulate the balance between fatty acid oxidation and synthesis, ensuring that cells have enough energy while preventing excessive accumulation of lipids.

Deficiencies or mutations in COAT can lead to various metabolic disorders, such as carnitine palmitoyltransferase I deficiency (CPT I deficiency), which may cause symptoms like muscle weakness, hypoglycemia, and cardiomyopathy. Proper diagnosis and management of these conditions often involve dietary modifications, supplementation with carnitine, and avoidance of fasting to prevent metabolic crises.

Diethylhexyl Phthalate (DEHP) is a type of phthalate compound that is commonly used as a plasticizer, a substance added to plastics to make them more flexible and durable. DEHP is a colorless, oily liquid with an odor similar to oil or benzene. It is soluble in organic solvents but not in water.

DEHP is used primarily in the production of polyvinyl chloride (PVC) plastics, such as flexible tubing, hoses, and medical devices like blood bags and intravenous (IV) lines. DEHP can leach out of these products over time, particularly when they are subjected to heat or other stressors, leading to potential human exposure.

Exposure to DEHP has been linked to a variety of health effects, including reproductive toxicity, developmental and neurological problems, and an increased risk of cancer. As a result, the use of DEHP in certain applications has been restricted or banned in some countries. The medical community is also moving towards using alternative plasticizers that are considered safer for human health.

Cholestyramine resin is a medication used to treat high levels of cholesterol in the blood. It is a type of drug called a bile acid sequestrant, which works by binding to bile acids in the digestive system and preventing them from being reabsorbed into the body. This leads to an increased removal of cholesterol from the body, which can help lower the levels of cholesterol in the blood.

Cholestyramine resin is available as a powder that is mixed with water or other fluids and taken by mouth. It may be used alone or in combination with other medications to treat high cholesterol. In addition to its use for lowering cholesterol, cholestyramine resin may also be used to treat itching associated with partial biliary obstruction (blockage of the bile ducts) and to reduce the absorption of certain drugs, such as digitalis and thyroid hormones.

It is important to follow the instructions of a healthcare provider when taking cholestyramine resin, as the medication can interfere with the absorption of other medications and nutrients. It may also cause gastrointestinal side effects, such as constipation, bloating, and gas.

I could not find a medical definition specifically for "Cocos." However, Cocos is a geographical name that may refer to:

* The Cocos (Keeling) Islands, an Australian territory in the Indian Ocean.
* Cocos nucifera, the scientific name for the coconut palm tree.

There are some medical conditions related to the consumption of coconuts or exposure to the coconut palm tree, such as allergies to coconut products, but there is no specific medical term "Cocos."

Anticholesteremic agents are a class of medications that are used to lower the levels of cholesterol and other fats called lipids in the blood. These medications work by reducing the production of cholesterol in the body, increasing the removal of cholesterol from the bloodstream, or preventing the absorption of cholesterol in the digestive tract.

There are several types of anticholesteremic agents, including:

1. Statins: These medications work by blocking a liver enzyme that is necessary for the production of cholesterol. Examples of statins include atorvastatin, simvastatin, and rosuvastatin.
2. Bile acid sequestrants: These medications bind to bile acids in the digestive tract and prevent them from being reabsorbed into the bloodstream. This causes the liver to produce more bile acids, which in turn lowers cholesterol levels. Examples of bile acid sequestrants include cholestyramine and colesevelam.
3. Nicotinic acid: Also known as niacin, this medication works by reducing the production of very low-density lipoproteins (VLDL) in the liver, which are a major source of bad cholesterol.
4. Fibrates: These medications work by increasing the removal of cholesterol from the bloodstream and reducing the production of VLDL in the liver. Examples of fibrates include gemfibrozil and fenofibrate.
5. PCSK9 inhibitors: These are a newer class of medications that work by blocking the action of a protein called PCSK9, which helps regulate the amount of cholesterol in the blood. By blocking PCSK9, these medications increase the number of LDL receptors on the surface of liver cells, which leads to increased removal of LDL from the bloodstream.

Anticholesteremic agents are often prescribed for people who have high cholesterol levels and are at risk for heart disease or stroke. By lowering cholesterol levels, these medications can help reduce the risk of heart attack, stroke, and other cardiovascular events.

Bezafibrate is a medication that belongs to a class of drugs called fibrates. It is primarily used to treat high cholesterol and related conditions, such as hyperlipidemia and mixed dyslipidemia. The medication works by reducing the levels of triglycerides and increasing the levels of "good" cholesterol (HDL) in the blood.

Bezafibrate achieves this effect by activating certain receptors in the body, known as peroxisome proliferator-activated receptors (PPARs), which play a role in regulating lipid metabolism. By binding to these receptors, bezafibrate helps to promote the breakdown of fats and reduce the production of cholesterol in the liver.

It is important to note that bezafibrate should be used in conjunction with lifestyle modifications, such as a healthy diet and regular exercise, to effectively manage high cholesterol and related conditions. Additionally, it may interact with other medications, so it is essential to inform your healthcare provider of all the drugs you are taking before starting bezafibrate therapy.

As with any medication, bezafibrate can cause side effects, including gastrointestinal symptoms such as nausea, diarrhea, and abdominal pain, as well as headaches, muscle cramps, and skin rashes. In rare cases, it may also cause more serious side effects, such as liver or kidney damage, so regular monitoring of liver and kidney function is recommended during treatment.

Overall, bezafibrate is a valuable tool in the management of high cholesterol and related conditions, but it should be used under the guidance and supervision of a healthcare professional to ensure safe and effective use.

Phototherapy is a medical treatment that involves the use of light to manage or improve certain conditions. It can be delivered in various forms, such as natural light exposure or artificial light sources, including lasers, light-emitting diodes (LEDs), or fluorescent lamps. The wavelength and intensity of light are carefully controlled to achieve specific therapeutic effects.

Phototherapy is most commonly used for newborns with jaundice to help break down bilirubin in the skin, reducing its levels in the bloodstream. This type of phototherapy is called bilirubin lights or bili lights.

In dermatology, phototherapy can be applied to treat various skin conditions like psoriasis, eczema, vitiligo, and acne. Narrowband ultraviolet B (UVB) therapy, PUVA (psoralen plus UVA), and blue or red light therapies are some examples of dermatological phototherapies.

Phototherapy can also be used to alleviate symptoms of seasonal affective disorder (SAD) and other mood disorders by exposing patients to bright artificial light, which helps regulate their circadian rhythms and improve their mood. This form of phototherapy is called light therapy or bright light therapy.

It's essential to consult a healthcare professional before starting any phototherapy treatment, as inappropriate use can lead to adverse effects.

Acyl-CoA oxidase is an enzyme that plays a crucial role in the breakdown of fatty acids within the body. It is located in the peroxisomes, which are small organelles found in the cells of living organisms. The primary function of acyl-CoA oxidase is to catalyze the initial step in the beta-oxidation of fatty acids, a process that involves the sequential removal of two-carbon units from fatty acid molecules in the form of acetyl-CoA.

The reaction catalyzed by acyl-CoA oxidase is as follows:

acyl-CoA + FAD → trans-2,3-dehydroacyl-CoA + FADH2 + H+

In this reaction, the enzyme removes a hydrogen atom from the fatty acyl-CoA molecule and transfers it to its cofactor, flavin adenine dinucleotide (FAD). This results in the formation of trans-2,3-dehydroacyl-CoA, FADH2, and a proton. The FADH2 produced during this reaction can then be used to generate ATP through the electron transport chain, while the trans-2,3-dehydroacyl-CoA undergoes further reactions in the beta-oxidation pathway.

There are two main isoforms of acyl-CoA oxidase found in humans: ACOX1 and ACOX2. ACOX1 is primarily responsible for oxidizing straight-chain fatty acids, while ACOX2 specializes in the breakdown of branched-chain fatty acids. Mutations in the genes encoding these enzymes can lead to various metabolic disorders, such as peroxisomal biogenesis disorders and Refsum disease.

Transcription initiation, genetic is the process by which the transcription of a gene is initiated. It is the first step in gene expression, where the information encoded in DNA is copied into RNA. This process involves the unwinding of the double-stranded DNA at the promoter region of the gene, followed by the recruitment of the RNA polymerase enzyme and other transcription factors to the promoter site. Once assembled, the RNA polymerase begins to synthesize an RNA copy of the gene's sequence, starting from the transcription start site (TSS). This RNA molecule, known as messenger RNA (mRNA), will then be translated into a protein or used to produce non-coding RNAs with various functions. Transcription initiation is tightly regulated and can be influenced by various factors such as promoter strength, transcription factor availability, and chromatin structure.

PPAR-alpha (Peroxisome Proliferator-Activated Receptor alpha) is a type of nuclear receptor protein that functions as a transcription factor, regulating the expression of specific genes involved in lipid metabolism. It plays a crucial role in the breakdown of fatty acids and the synthesis of high-density lipoproteins (HDL or "good" cholesterol) in the liver. PPAR-alpha activation also has anti-inflammatory effects, making it a potential therapeutic target for metabolic disorders such as diabetes, hyperlipidemia, and non-alcoholic fatty liver disease (NAFLD).

"Valerates" is not a recognized medical term. However, it may refer to a salt or ester of valeric acid, which is a carboxylic acid with the formula CH3CH2CH2CO2H. Valeric acid and its salts and esters are used in pharmaceuticals and perfumes. Valerates can have a sedative effect and are sometimes used as a treatment for anxiety or insomnia. One example is sodium valerate, which is used in the manufacture of some types of medical-grade polyester. Another example is diethyl valerate, an ester of valeric acid that is used as a flavoring agent and solvent.

Enzyme induction is a process by which the activity or expression of an enzyme is increased in response to some stimulus, such as a drug, hormone, or other environmental factor. This can occur through several mechanisms, including increasing the transcription of the enzyme's gene, stabilizing the mRNA that encodes the enzyme, or increasing the translation of the mRNA into protein.

In some cases, enzyme induction can be a beneficial process, such as when it helps the body to metabolize and clear drugs more quickly. However, in other cases, enzyme induction can have negative consequences, such as when it leads to the increased metabolism of important endogenous compounds or the activation of harmful procarcinogens.

Enzyme induction is an important concept in pharmacology and toxicology, as it can affect the efficacy and safety of drugs and other xenobiotics. It is also relevant to the study of drug interactions, as the induction of one enzyme by a drug can lead to altered metabolism and effects of another drug that is metabolized by the same enzyme.

... 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 ...
So clofibride, just like clofibrate is a prodrug of clofibric acid. "Clofibride". Entry on Clofibrat. at: Römpp Online. Georg ... Clofibride is a derivative of clofibrate. In the body it is converted into 4-chlorophenoxyisobutyric acid (clofibric acid), ...
Formation of clofibrate mercapturate in humans". Drug Metabolism and Disposition. 10 (6): 609-13. PMID 6130909. "Two Named 2017 ...
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 ...
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- ...
Both dose levels of estrogen as well as clofibrate were also found to increase the incidence of gallbladder disease in the ... Stamler J (1977). "The Coronary Drug Project --- Findings with Regard to Estrogen, Dextrothyroxine, Clofibrate and Niacin". Adv ... clofibrate (1.8 g/day), dextrothyroxine (6 mg/day), niacin (3 g/day), and placebo (lactose 3.8 mg/day). The high-dose estrogen ...
"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 ...
... was first synthesized in 1974, as a derivative of clofibrate, and was initially offered in France. It was initially ...
Estrogen, tamoxifen, heroin, methadone, clofibrate, 5-flurouracile, mitotane, and perphenazine all increase thyroid binding ...
Aluminium clofibrate Bezafibrate Ciprofibrate Choline fenofibrate Clinofibrate Clofibrate Clofibride Fenofibrate Gemfibrozil ...
... 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 ...
Treatment consisted mainly of dietary measures, such as a low-fat diet, and poorly tolerated medicines, such as clofibrate, ...
... induction of superoxide dismutase and ascorbate peroxidase correlates with high H2O2 concentration in seawater from clofibrate- ...
... effects of dietary restriction of very long chain fatty acids and of administration of carnitine and clofibrate on clinical ...
Prior to the introduction of the statins, clofibrate (an older fibrate that often caused gallstones), probucol (especially in ...
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 ( ...
... clofibrate, gemfibrozil, ciprofibrate, bezafibrate, and fenofibrate). They were originally indicated for dyslipidemia of ...
... clofibrate MeSH D02.241.081.160.225 - clofibric acid MeSH D02.241.081.160.225.133 - bezafibrate MeSH D02.241.081.160.225.187 - ... clofenapate MeSH D02.241.081.160.225.195 - clofibrate MeSH D02.241.081.160.225.396 - gemfibrozil MeSH D02.241.081.160.225.597 ...
Pulmonary causes Infection Pneumonia Lung abscess Asthma Cystic fibrosis Drugs Chlorpropamide Clofibrate Phenothiazine ...
... and spironolactone Additional medications for high cholesterol such as clofibrate, fenofibrate, gemfibrozil, and niacin (when ...
Cerivastatin C10AA07 Rosuvastatin C10AA08 Pitavastatin C10AB01 Clofibrate C10AB02 Bezafibrate C10AB03 Aluminium clofibrate ...
... 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 ...
Clofibrate impairs absorption of vitamin B122. • Individuals taking clofibrate should avoid supplementing iron, or using multi- ... Clofibrate. side effects, nutrient depletions, herbal interactions and health notes:. Data provided by Applied Health. • The ... Clofibrate. Clonazepam. Clonidine. Clozaril. Codeine. Cognex. Colazal. Colchicine. Colestid. Colestipol. Combivent. Compazine. ... Clofibrate-induced alterations in zinc, iron and copper metabolism. Biochem Pharmacol 1978 Jan 1;27(1):125-127.. 3 Powanda MC, ...
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Gemifibrozil is closely related to clofibrate have the same potential side effects and health risk for toxicity, including gall ... blood clotting and angina have been reported in people taking clofibrate. Gemifibrozil is closely related to clofibrate and so ... Clofibrate Side Effects: Gemfibrozil Adverse Effects On Triglycerides. Question: What adverse effects happen to people who take ... Clofibrate and gemifibrozil can be prescribed to people who have high triglyceride level due to genetic disorder say about ...
a drug (trade name Atromid-S) that reduces lipids in the blood serum. ...
克羅纖維化 CLOFIBRATE ARCANA / 抗膽醇血症 / 藥要看提供 ... CLOFIBRATE "ARCANA" 藥品類別. 01製劑原料 管制藥
Molecular dynamics simulation of palmitoyel - co a hydrolase interaction with fmn ، clofibrate و 2, 4- dichlorophenoxy acetic ...
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).
clofibrate. Corticosteroids (used to treat inflammation). *dexamethasone (DMSO). *hydrocortisone. Diabetes medications. * ...
The syndrome of inappropriate antidiuretic hormone (ADH) secretion (SIADH) is defined by the hyponatremia and hypo-osmolality resulting from inappropriate, continued secretion or action of the hormone despite normal or increased plasma volume, which results in impaired water excretion. The key to understanding the pathophysiology, signs, symp...
With the development of world economies and the continuous improvement of living standards, pharmaceutical and personal care products (PPCPs) have attracted significant attention because of their widespread detection in wastewater and the natural environment. Their biological toxicity, environmental persistence, and other hazardous characteristics might pose a threat to the ecological environment and human health. How to treat source-separated urine as a valuable recyclable resource has become a novel challenge. In this review, we briefly described the sources of pharmaceuticals, explored the various metabolic pathways of pharmaceuticals, and concluded that urinary excretion is the primary metabolic pathway of pharmaceuticals. Next, the current status of pharmaceutical contamination in human urine, sewage plants, and surface water was summarized. It is shown that the concentration of pharmaceuticals in human urine is usually 2-3 orders of magnitude higher than that in sewage plants and surface water.
Using this medicine while you are pregnant can harm your unborn baby. Use an effective form of birth control to keep from getting pregnant. If you think you have become pregnant while using the medicine, tell your doctor right away. Do not use this medicine if you are also taking any of the following medicines: boceprevir (Victrelis®), cobicistat-containing products (Stribild®), cyclosporine (Gengraf®, Neoral®, Sandimmune®), danazol (Danocrine®), gemfibrozil (Lopid®), nefazodone (Serzone®), telaprevir (Incivek®), certain antibiotics (such as clarithromycin, erythromycin, itraconazole, ketoconazole, posaconazole, telithromycin, voriconazole, Nizoral®), or medicines to treat HIV/AIDS (such as atazanavir, indinavir, nelfinavir, ritonavir, saquinavir, tipranavir, Crixivan®, Kaletra®, Lexiva®, Norvir®, Prezista®, Reyataz®). Using these medicines together with sitagliptin and simvastatin combination may increase your risk of muscle injury and could result in kidney problems. Chinese ...
SKU: 1-01454 Category: Other Chiral Synthons & APIs & Intermediates Tag: H Cas No. : [517-28-2][1412-19-7 517292] Mol Formula : C16H14O6 . 3 H2O Fw : Fw 356.33 Properties 1 : mp 100 - 120°C ...
SKU: 9-10302 Category: Other Diagnostic Probes Reagents Tag: C Cas No. : [501-53-1] Synonym / Description : Benzyl chloroformate, Cbz-Cl Mol Formula : C8H7ClO3 Fw : Fw 170.60 ...
Increase in hepatic pyruvate (glyoxylate) aminotransferase activity on administration of clofibrate to the rat. ... aminotransferase activity on administration of clofibrate to the rat. Together they form a unique fingerprint. ...
Microsomes Clofibrate, Male Rat liver , MBS657660 , MyBiosourceProduct Short Name: [Microsomes Clofibrate, Male Rat liver] ...
Clofibrate Estrogen-containing oral contraceptives Estrogens (oral) Heroin / Methadone 5-Fluorouracil Mitotane Tamoxifen ...
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 ... Clofibrate Treatment Decreases Inflammation and Reverses Myocardial Infarction-Induced Remodelation in a Rodent Experimental ...
... clofibrate (62.5 mg/kg of BW), or fish oil (250 mg/kg of BW). Calves treated with clofibrate consumed less dry matter. Body ... Animals, Cattle, Clofibrate, Fatty Acids, Fish Oils, Gene Expression Regulation, Hypolipidemic Agents, Lipids, Liver, Liver ... Clofibrate increased or tended to increase liver expression of several PPARalpha target genes involved in fatty acid oxidation ... In liver slices incubated for 8 h, conversion of palmitate to CO(2) was greater for calves treated with clofibrate compared ...
Clofibrate Estrogen containing oral contraceptives. Estrogens (oral). Heroin / Methadone. 5-Fluorouracil. Mitotane. Tamoxifen. ...
clofibrate multiple interactions. ISO. RGD:1323827. 6480464. [Clofibrate co-treated with Acetaminophen] affects the expression ... Clofibrate co-treated with Acetaminophen] affects the expression of MC1R mRNA, PPARA affects the reaction [[Clofibrate co- ... of MC1R mRNA, PPARA affects the reaction [[Clofibrate co-treated with Acetaminophen] affects the expression of MC1R mRNA]. CTD ...
Clofibrate. Ascalan. Doxazosin Mesylate. Ascorbisal. Aspirin; Vitamin C (Ascorbic Acid). Atenolan. Atenolol. ...
... clofibrate. The Coronary Drug Project was a 6-year randomized, double-blind study involving 1000 clofibrate, 1000 nicotinic ... Both clofibrate and gemfibrozil may increase cholesterol excretion into the bile, leading to cholelithiasis. If cholelithiasis ... There was no difference in mortality between the clofibrate-treated subjects and 3000 placebo-treated subjects, but twice as ... There was a statistically significant (44%) higher age-adjusted total mortality in the clofibrate-treated group than in a ...
Clofibrate 10. Insulin (Novolin) Related Therapies and Procedures. 1. Transplantation (Transplant Recipients) ...
clofibrate a lipid-lowering drug that is used to reduce high levels of fat and cholesterol. ...
  • Estrogens, oral contraceptives, clofibrate, other lipid-lowering drugs may reduce effectiveness of ursodiol by increasing hepatic cholesterol secretion. (empr.com)
  • Subject has consumed medicines or foodstuff that may affect pharmacological or pharmacokinetic properties of chenodeoxycholic acid (for example: Antacids (aluminum containing), Bile acid sequestrants such as (cholestyramine or colestipol), Clofibrate, Coumarin-derivative anticoagulants, Estrogens & oral contraceptive) two weeks before dosing, during the study and two weeks after dosing. (who.int)
  • Essential hyperlipemia with xanthomatosis: effects of cholestyramine and clofibrate. (naturalnews.com)
  • About half the deaths with clofibrate were due to malignancies such as liver cancer. (tandurust.com)
  • In liver slices incubated for 8 h, conversion of palmitate to CO(2) was greater for calves treated with clofibrate compared with control calves or calves treated with fish oil. (oregonstate.edu)
  • Clofibrate increased or tended to increase liver expression of several PPARalpha target genes involved in fatty acid oxidation (e.g. (oregonstate.edu)
  • Overall, our data indicated that bovine liver responded to clofibrate treatment but not fish oil, although increases in hepatic lipid metabolism were much less than those reported in rodents treated with clofibrate or fish oil. (oregonstate.edu)
  • 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-induced alterations in serum protein patterns. (naturalnews.com)
  • Effects of the peroxisome proliferator-activated receptor-alpha agonists clofibrate and fish oil on hepatic fatty acid metabolism in weaned dairy calves. (oregonstate.edu)
  • Clofibrate was discontinued in 2002 due to adverse effects. (wikipedia.org)
  • Question: What adverse effects happen to people who take clofibrate and gemifibrozil? (tandurust.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)
  • Gemifibrozil is prescribed more often than clofibrate and it may also be used to prevent the development of heart disease in people with a combination of high LDL cholesterol, high triglycerides and low HDL cholesterol. (tandurust.com)
  • Clofibrate Treatment Decreases Inflammation and Reverses Myocardial Infarction-Induced Remodelation in a Rodent Experimental Model. (bvsalud.org)
  • 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. (bvsalud.org)
  • clofibrate treatment raised those parameters to control values. (bvsalud.org)
  • n=15) were assigned to 1 of 3 groups for a 5-d treatment period: control (untreated), clofibrate (62.5 mg/kg of BW), or fish oil (250 mg/kg of BW). (oregonstate.edu)
  • An increase in heart arrhythmia (loss of rhythmic heartbeat), blood clotting and angina have been reported in people taking clofibrate. (tandurust.com)
  • Clofibrate and gemifibrozil can be prescribed to people who have high triglyceride level due to genetic disorder say about 2000mg/dL or more. (tandurust.com)
  • 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). (bvsalud.org)
  • 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 is a fibric acid derivative used in the therapy of hypertriglyceridemia and dyslipidemia. (nih.gov)
  • Clofibrate, like other fibrates, decreases elevated blood lipids (triglycerides and cholesterol) by increasing the activity of lipases that catabolize triglyceride-rich lipoproteins and slightly decreasing cholesterol biosynthesis (Miller 1998). (e-lactancia.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)
  • Tumour radiosensitization by clofibrate and its analogs: possible mechanisms. (thieme-connect.com)
  • Expression changes in genes involved in fatty acid metabolism (e.g., acyl-CoA oxidase), cell proliferation (e.g., topoisomerase II-Alpha), and fatty acid oxidation (e.g., cytochrome P450 4A1), consistent with the mechanism of clofibrate hepatotoxicity, were detected. (nih.gov)
  • Assessment of Preclinical Liver and Skeletal Muscle Biomarkers Following Clofibrate Administration in Wistar Rats. (nih.gov)
  • As part of a series of studies conducted by the International Life Sciences Institute Health and Environmental Science Institute Technical Committee on the Application of Genomics to Mechanism-Based Risk Assessment, the biological response in rats to the hepatotoxin clofibrate was investigated. (nih.gov)
  • Clofibrate Treatment Decreases Inflammation and Reverses Myocardial Infarction-Induced Remodelation in a Rodent Experimental Model. (bvsalud.org)
  • In conclusion, clofibrate decreases cardiac remodeling , decreases inflammatory molecules, and partly preserves myocardial diameters. (bvsalud.org)
  • Due to increased mortality and other serious complications in patients treated with Clofibrate (Oliver 2012, WHO 1984), in most countries the product has been withdrawn from sale or restrictions have been imposed on its approved use. (e-lactancia.org)
  • Clofibrate-induced gene expression changes in rat liver: a cross-laboratory analysis using membrane cDNA arrays. (nih.gov)
  • An antilipemic agent that is the biologically active metabolite of CLOFIBRATE . (bvsalud.org)
  • Seven days post-MI, animals were further divided to receive vehicle (V) or clofibrate (100 mg/kg, C) for 7 days. (bvsalud.org)