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Tricor (Fenofibrate)

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Tricor is the medication of high quality, which is taken in treatment of high triglyceride levels and high cholesterol with diet changes. Tricor is acting by increasing enzyme which breaks down fats in the blood. It is fibrate (lipid-lowering agent).

Other names for this medication:
Antara, Antilip, Apteor, Catalip, Controlip, Craveril, Docfenofi, Durafenat, Einecs, Elipsia, Evothyl, Febira, Fegenor, Felosma, Fenobeta, Fenobrat, Fenobrate, Fenocap, Fenofib, Fenofibrat, Fenofibrate, Fenofibrato, Fenofibratum, Fenofix, Fenogal, Fenoglide, Fenohexal, Fenolid, Fenolip, Fenoratio, Fenosup, Fenox, Fibrafen, Fibral, Fulcro, Grofibrat, Hafenthyl, Hyperchol, Katalip, Lexemin, Lifen, Lifibrat, Lipanthyl, Lipantil, Liparison, Lipcor, Liperial, Lipicard, Lipidcare, Lipidil, Lipidof, Lipilfen, Lipirate, Lipired, Lipirex, Lipivim, Lipofen, Lipofene, Lipofib, Lipohexal, Lipolin, Lipsin, Lofat, Lofibra, Lowlip, Minuslip, Naftilan, Nofiate, Nolipax, Normalip, Normolip, Nubrex, Nuozhituo, Phenofibrate, Procetofen, Procetoken, Proctofene, Secalip, Stanlip, Supralip, Suprelip, Tilene, Trigent, Triglide, Trilipix, Trolip, Versamid, Xafenor, Yosenob, Zumafib

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Also known as:  Fenofibrate.


Tricor is the medication of high quality, which is taken in treatment of high triglyceride levels and high cholesterol with diet changes.

The target of this perfect remedy is the treatment of high triglyceride levels and high cholesterol with diet changes.

Tricor is also known as Fenofibrate, Fenofibric acid, Lipicard, Lofibra, Lipanthyl, Fenocor-67.

Tricor is acting by increasing enzyme which breaks down fats in the blood. It is fibrate (lipid-lowering agent).

Generic name of Tricor is Fenofibrate.

Brand names of Tricor are Tricor, Tricor, Antara, Triglide, Lofibra, Lipofen.


Tricor can be taken once a day. Take Tricor capsules orally with water at the same time every day, with food.

If you are taking colestipol (such as Colestid) or cholestyramine (such as Questran) while using Tricor you should take these medicines at least 1 hour after using Tricor or 4-6 hours before using Tricor.

Follow low-fat diet, low-cholesterol.

If you want to achieve most effective results do not stop taking Tricor suddenly.


If you overdose Tricor and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Tricor if you are allergic to its components.

Do not take Tricor if you're pregnant or you plan to have a baby, or you are a nursing mother. Tricor can ham your baby.

Be careful with Tricor if you suffer from liver cirrhosis, hepatitis, severe kidney disease, gallbladder disease, diabetes, kidney, liver, heart disease, hypothyroidism.

Be careful with Tricor if you are taking such medicines as blood thinner (warfarin (such as Coumadin)); fluvastatin (such as Lescol), cholesterol-lowering medicines (lovastatin (such as Mevacor), simvastatin (such as Zocor), cerivastatin (such as Baycol), pravastatin (such as Pravachol), atorvastatin (such as Lipitor), cyclosporine (such as Gengraf, Neoral, Sandimmune).

If you experience drowsiness and dizziness while taking Tricor you should avoid any activities such as driving or operating machinery.

Avoid alcohol.

Elderly people should be very careful with Tricor.

Keep low-cholesterol and low-fat diet.

Do not stop taking Tricor suddenly.

tricor generic medication

The mRNA expression and protein activity of PAI-1 was significantly induced by linoleic acid, but was obviously suppressed by fenofibrate. In the HepG-2 cells transfected with PAI-pCAT promoter constructs the PAI-1 transcription activity was significantly induced by linoleic acid, but suppressed by fenofibrate. The level of PAI-1 transcription was also significantly increased when co-transfected with PAI-pCAT promoter construct and PPAR alpha-pSG5 expression plasmid to HepG-2 cells. Furthermore, in the condition of transfection with NF-kappaB-response element-deletion-pCAT construct, both linoleic acid and fenofibrate increased the PAI-1 transcriptional activity, whereas in those cells transfected with VLDL/fatty acid response element-deletion-pCAT construct, fenofibrate significantly reduced PAI-1 transcriptional activity, but no change in PAI-1 transcription activity was found with linoleic acid stimulation.

tricor 96 mg

Fifty-six patients were given atorvastatin 10 mg and placebo, atorvastatin 10 mg and fenofibrate 200 mg, or fenofibrate 200 mg and placebo daily during each two-month treatment period of a randomized, double-blind, placebo-controlled crossover trial with two washout periods of two months' each.

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Multiple clinical research facilities in the US and Canada.

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To investigate the fat decreasing effects of fenofibrate on alcoholic fatty liver and drug-induced fatty liver in rats.

tricor 215 mg

To investigate the relationship of inflammation and endothelial activation with insulin resistance and adiposity in type 2 diabetes.

tricor dose

Rosuvastatin, a new statin, has been shown to possess a number of advantageous pharmacological properties, including enhanced HMG-CoA reductase binding characteristics, relative hydrophilicity, and selective uptake into/activity in hepatic cells. Cytochrome p450 (CYP) metabolism of rosuvastatin appears to be minimal and is principally mediated by the 2C9 enzyme, with little involvement of 3A4; this finding is consistent with the absence of clinically significant pharmacokinetic drug-drug interactions between rosuvastatin and other drugs known to inhibit CYP enzymes. Dose-ranging studies in hypercholesterolemic patients demonstrated dose-dependent effects in reducing low-density lipoprotein cholesterol (LDL-C) (up to 63%), total cholesterol, and apolipoprotein (apo) B across a 1- to 40-mg dose range and a significant 8.4% additional reduction in LDL-C, compared with atorvastatin, across the dose ranges of the two agents. Rosuvastatin has also been shown to be highly effective in reducing LDL-C, increasing high-density lipoprotein cholesterol (HDL-C), and producing favorable modifications of other elements of the atherogenic lipid profile in a wide range of dyslipidemic patients. In patients with mild to moderate hypercholesterolemia, rosuvastatin has been shown to produce large decreases in LDL-C at starting doses, thus reducing the need for subsequent dose titration, and to allow greater percentages of patients to attain lipid goals, compared with available statins. The substantial LDL-C reductions and improvements in other lipid measures with rosuvastatin treatment should facilitate achievement of lipid goals and reduce the requirement for combination therapy in patients with severe hypercholesterolemia. In addition, rosuvastatin's effects in reducing triglycerides, triglyceride-containing lipoproteins, non-HDL-C, and LDL-C and increasing HDL-C in patients with mixed dyslipidemia or elevated triglycerides should be of considerable value in enabling achievement of LDL-C and non-HDL-C goals in the numerous patients with combined dyslipidemias or metabolic syndrome who require lipid-lowering therapy. Rosuvastatin is well tolerated alone, and in combination with fenofibrate, extended-release niacin, and cholestyramine, and has a safety profile similar to that of currently marketed statins. A large, long-term clinical trials program is under way to investigate the effects of rosuvastatin on atherosclerosis and cardiovascular morbidity and mortality.

tricor cholesterol medicine

We measured the thickness of the intima media layer of the carotid artery, a strong predictor of the risk of future vascular events, in 397 Type 2 diabetic patients drawn from the Fenofibrate Intervention and Event Lowering in Diabetes study, prior to treatment allocation.

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Restoration of the disturbed ET-1 mRNA/NOS mRNA balance by lipanthyl might be one of its mechanisms leading to regression of atherosclerosis.

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Fenofibrate is a synthetic ligand for the nuclear receptor peroxisome proliferator-activated receptor (PPAR) alpha and has been widely used in the treatment of metabolic disorders, especially hyperlipemia, due to its lipid-lowering effect. The molecular mechanism of lipid-lowering is relatively well defined: an activated PPARalpha forms a PPAR-RXR heterodimer and this regulates the transcription of genes involved in energy metabolism by binding to PPAR response elements in their promoter regions, so-called "trans-activation". In addition, fenofibrate also has anti-inflammatory and anti-athrogenic effects in vascular endothelial and smooth muscle cells. We have limited information about the anti-inflammatory mechanism of fenofibrate; however, "trans-repression" which suppresses production of inflammatory cytokines and adhesion molecules probably contributes to this mechanism. Furthermore, there are reports that fenofibrate affects endothelial cells in a PPARalpha-independent manner. In order to identify PPARalpha-dependently and PPARalpha-independently regulated transcripts, we generated microarray data from human endothelial cells treated with fenofibrate, and with and without siRNA-mediated knock-down of PPARalpha. We also constructed dynamic Bayesian transcriptome networks to reveal PPARalpha-dependent and -independent pathways. Our transcriptome network analysis identified growth differentiation factor 15 (GDF15) as a hub gene having PPARalpha-independently regulated transcripts as its direct downstream children. This result suggests that GDF15 may be PPARalpha-independent master-regulator of fenofibrate action in human endothelial cells.

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Schisandrin B, an active ingredient isolated from the fruit of Schisandra chinensis, increased serum and hepatic triglyceride levels in mice. In the present study, the effective kinetics of schisandrin B on serum/hepatic triglyceride and total cholesterol levels in mice without and with the influence of fenofibrate were investigated. Parameters on hepatic index (the ratio of liver weight to body weight × 100) were also analyzed. Mice were intragastrically treated with schisandrin B at a single dose of 0.2, 0.4, 0.8, or 1.6 g/kg, without or with fenofibrate pretreatment (0.1 g/kg/day for 4 days, p.o.). Twenty-four hours after schisandrin B treatment, serum/hepatic triglyceride and total cholesterol levels were measured. Schisandrin B treatment dose-dependently increased serum and hepatic triglyceride levels as well as hepatic index in mice. In contrast, hepatic total cholesterol levels were decreased in a dose-dependent manner in schisandrin B-treated mice. Data obtained from effective kinetics analysis indicated that the action of schisandrin B on serum triglyceride had a higher specificity than those on hepatic total cholesterol and hepatic index. While fenofibrate pretreatment inhibited the schisandrin B-induced elevation in serum triglyceride levels, it completely abrogated the elevation of hepatic triglyceride levels in schisandrin B-treated mice. The combined treatment with schisandrin B and fenofibrate decreased hepatic total cholesterol level and increased the hepatic index in an additive or semi-additive manner, respectively. In conclusion, the results of effective kinetics analysis indicated that the schisandrin B-induced hypertriglyceridemia was competitively inhibited by fenofibrate. Schisandrin B may offer the prospect of setting up a mouse model of hypertriglyceridemia and fatty liver for screening triglyceride-lowering drug candidates.

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Preclinical evaluation of DRF 2655, a peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARgamma agonist, as a body-weight lowering, hypolipidemic and euglycemic agent.

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A prospective, open-label, randomised study in non-diabetic patients (n = 186) with MetS (follow-up: 54 weeks). All patients had both biochemical and ultrasonographic evidence of NAFLD at baseline. Other causes of liver disease were excluded. Patients received lifestyle advice and treatment for hypertension (mainly inhibitors of the renin-angiotensin system), impaired fasting glucose (metformin), obesity (orlistat) and dyslipidaemia [randomly allocated to atorvastatin 20 mg/day (n = 63) or micronised fenofibrate 200 mg/day (n = 62) or both drugs (n = 61)]. Liver ultrasonography was assessed at baseline and at the end of the study.

tricor 600 mg

Collagenous repeat containing sequence of 26-kDa protein (CORS-26) was identified as a new gene transcript expressed in cartilage with unknown function. It was the aim of this study to investigate expression, regulation, and function of CORS-26 in adipocytes.

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In humans, fibrates are frequently used normolipidemic drugs. Fibrates act by regulating genes involved in lipoprotein metabolism via activation of the peroxisome proliferator-activated receptor-alpha (PPARalpha) in liver. In rodents, however, fibrates induce a peroxisome proliferation, leading to hepatomegaly and possibly hepatocarcinogenesis. Although this peroxisome proliferative response appears not to occur in humans, it remains controversial whether the beneficial effects of fibrates on lipoprotein metabolism can occur dissociated from such undesirable peroxisomal response. Here, we assessed the influence of fenofibrate on lipoprotein metabolism and peroxisome proliferation in the rabbit, an animal that, contrary to rodents and similar to humans, is less sensitive to peroxisome proliferators.

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tricor brand communications 2017-04-30

After the treatment, the total cholesterol, high-density-lipoprotein cholesterol (HDL-C), non HDL-C, low-density-lipoprotein cholesterol (LDL-C), and triglyceride were comparable between the 2 groups. The change in the non-HDL-C were -7.39 ± 26.58 (- Lanoxin Prices 6.62%) and -0.68 ± 24.49 (-1.19%) mg/dl (p = 0.28); and the change in the triglyceride were -36.61 ± 62.51 (-14.00%) and -44.77 ± 77.35 (-23.17%) mg/dl (p = 0.64), respectively. While 41.37% of group A and 38.69% of group B achieved their LDL-C goal (< 100 mg/dl) (p = 0.79), 37.26% of group A and 42.31% of group B achieved their triglyceride goal (< 150 mg/dl) (p = 0.53), respectively. The changes in the serum transaminase and creatinine phosphokinase were similar between the 2 groups.

tricor drug class 2017-06-06

These results show that fenofibrate decreases hepatic lipid synthesis through induction of CREBH. Cialis 5mg Tablet This study suggests CREBH as a novel negative regulator of SREBP-1c production and hepatic lipogenesis.

tricor mg 2015-04-15

Micronized fenofibrate is a potent hypolipidemic drug with only rare side effects. It is very good tolerated by the patients. Micronized fenofibrate is particularly prescribed for combined hyperlipidemia, however we can use it also in some patients with familial hypercholesterolemia. For to Prevacid Dose Newborn the treatment very resistant hyperlipoproteinemias we should consider combined drug therapy.

tricor 40 mg 2016-08-01

All of the electrosprayed nanospherule formulations had remarkably enhanced aqueous solubility and dissolution compared with free drug. Moreover, Labrafil M 2125, a surfactant, had a positive influence on the solubility and dissolution of the drug in the electrosprayed nanospherule. Increases were observed as the PVP/drug ratio increased to 4:1, but higher ratios gave no significant increases. In particular, an electrosprayed nanospherule composed of fenofibrate, PVP, and Labrafil M 2125 at the weight ratio of 1:4:0.5 resulted in a particle size Geodon Medication of <200 nm with the drug present in the amorphous state. It demonstrated the highest solubility (32.51±2.41 μg/mL), an excellent dissolution (~85% in 10 minutes), and an oral bioavailability ~2.5-fold better than that of the free drug. It showed similar oral bioavailability compared to the conventional solid dispersion.

tricor online 2017-08-29

EtFSC, but not AqFSC, significantly elevated hepatic triglyceride (TG) in mice fed with ND. Feeding mice with HFCBD increased serum total cholesterol (TC), high density lipoprotein (HDL) and Urispas Tablet Usage low density lipoprotein (LDL) levels as well as alanine aminotransferase (ALT) activity. Supplementation with AqFSC, EtFSC or fenofibrate significantly reduced hepatic TC and TG levels. However, AqFSC and EtFSC supplementation increased serum HDL and LDL levels in mice fed with HFCBD. Fenofibrate increased serum HDL and reduced serum LDL contents in hypercholesterolemic mice. EtFSC reduced, but fenofibrate elevated, serum ALT activity in both normal and hypercholesterolemic mice. While fenofibrate reduced serum TC, TG, and HDL levels in mice fed with ND, it increased serum HDL and reduced serum LDL and TC levels in mice fed with HFCBD. Hepatomegaly was found in normal and hypercholesterolemic mice fed with diet supplemented with fenofibrate.

tricor drug interactions 2016-03-17

Median survival time of recurrent Order Levitra Online embryonal brain tumors is short regardless of salvage chemotherapy used. An evolving alternative approach to conventional chemotherapy is to target neovascularization by interfering with tumor angiogenesis at various levels.

tricor cholesterol medicine 2017-12-20

Alirocumab undergoes target-mediated clearance via binding of proprotein convertase subtilisin/kexin type 9 (PCSK9). Statins increase PCSK9 levels; the effects of nonstatin lipid-lowering therapies are unclear. Every Cordarone Brand Name -4-weeks dosing of alirocumab may be appropriate for some patients in absence of background statin but is not yet approved.

tricor 20 mg 2017-06-16

To determine the incidence and predictors of, and effects of fenofibrate on silent myocardial infarction (MI) in a large contemporary cohort of patients with type 2 diabetes in the Fenofibrate Mobic Drug Meloxicam Intervention and Event Lowering in Diabetes (FIELD) study.

tricor medication 2015-06-03

The effect of fenofibrate (Lipanthyl) on the more important lipid levels has been examined in 58 female patients. The other diseases of the women have been treated as well. The drug moderated cholesterol level very successfully. In response to the drug the serum cholesterol, serum triglyceride and LDL-cholesterol values decreased and the HDL-cholesterol level increased. The long-term application of the drug Bactroban Nasal Cost was well tolerated by the women. The introduction of fenofibrate is recommended in particular in the treatment of those internal-gynaecological diseases and postmenopause in which the normal lipid levels may facilitate to reach the final goal of therapy.

tricor tabs 2017-04-12

HIV patients on antiretroviral therapy (ART) have a unique dyslipidemia [elevated triglycerides and non-high-density lipoprotein-cholesterol (HDL-C), low HDL-C] with insulin resistance (characterized by hypoadiponectinemia).

tricor 67 mg 2015-01-23

sICAM-1 levels were significantly higher in HLPIIa and HLPIIb patients (331 +/- 19 ng/ml and 423 +/- 23 ng/ml, respectively) compared with the control group (236 +/- 12 mg/ml). MCP-1 levels were also significantly higher in HLPIIa and HLPIIb patients (170 +/- 9 pg/ml and 183 +/- 15 pg/ml, respectively) compared with the control group (100 +/- 4 pg/ml). Fenofibrate (200 mg daily) significantly decreased sICAM-1 (by 17%) and MCP-1 levels (by 12.5%). Simvastatin (20 mg daily) caused a significant decrease (by 10.5%) in sICAM-1 levels only. Restriction in dietary lipids resulted in a significant decrease in the levels of cholesterol (8%), LDL cholesterol (14.9%) and ApoB (12.7%), which was accompanied by a significant decrease in the levels of sICAM-1 (8.7%) and MCP-1 (16.1%).

tricor 135 mg 2016-07-02

Peroxisome proliferator-activated receptor (PPAR)-α, a lipid-sensing transcriptional factor, serves an important role in lipotoxicity. We evaluated whether fenofibrate has a renoprotective effect by ameliorating lipotoxicity in the kidney. Eight-week-old male C57BLKS/J db/m control and db/db mice, divided into four groups, received fenofibrate for 12 weeks. In db/db mice, fenofibrate ameliorated albuminuria, mesangial area expansion and inflammatory cell infiltration. Fenofibrate inhibited accumulation of intra-renal free fatty acids and triglycerides related to increases in PPARα expression, phosphorylation of AMP-activated protein kinase (AMPK), and activation of Peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α)-estrogen-related receptor (ERR)-1α-phosphorylated acetyl-CoA carboxylase (pACC), and suppression of sterol regulatory element-binding protein (SREBP)-1 and carbohydrate regulatory element-binding protein (ChREBP)-1, key downstream effectors of lipid metabolism. Fenofibrate decreased the activity of phosphatidylinositol-3 kinase (PI3K)-Akt phosphorylation and FoxO3a phosphorylation in kidneys, increasing the B cell leukaemia/lymphoma 2 (BCL-2)/BCL-2-associated X protein (BAX) ratio and superoxide dismutase (SOD) 1 levels. Consequently, fenofibrate recovered from renal apoptosis and oxidative stress, as reflected by 24 hr urinary 8-isoprostane. In cultured mesangial cells, fenofibrate prevented high glucose-induced apoptosis and oxidative stress through phosphorylation of AMPK, activation of PGC-1α-ERR-1α, and suppression of SREBP-1 and ChREBP-1. Our results suggest that fenofibrate improves lipotoxicity via activation of AMPK-PGC-1α-ERR-1α-FoxO3a signaling, showing its potential as a therapeutic modality for diabetic nephropathy.

tricor generic 2017-09-17

The typical group demonstrated significantly greater TG reduction and HDL-C increment, ie, 56% vs, 21.3% (P < .005) and 21% vs. 7.6% (P = .001), respectively, compared with the mixed group. There was greater LDL-C reduction within the mixed group compared with the typical group 21.0% vs. 2.2% (P < .05). Endothelial dysfunction was present in both groups at baseline. After treatment, the typical group demonstrated significant improvement in resting brachial diameter (3.9 mm [interquartile range {IQR} 3.3-4.7] to 4.2 mm [IQR 3.4-4.8], P = .001) compared with no change within the mixed group (3.6 mm [IQR 3.1-5.4] to 3.7 mm [IQR 3.1-5.3], P = .26). Flow-mediated diameter improved significantly in both groups. The mixed group had significantly greater levels of hs-CRP at baseline but no changes throughout the study. The mixed group demonstrated an increase in vascular adhesion molecule-1 from 706 ng/mL (IQR 566-1195) to 845 ng/mL (637-1653; P = .01), a reduction of tumor necrosis factor-α from 7.0 pg/mL (IQR 1.0-43.5) to 2.5 pg/mL (IQR 1.5-13.5; P = .04) throughout the study.

tricor medicine 2015-08-31

Apolipoprotein E (apoE) is one of the major protein constituents of chylomicron and very low density lipoprotein (VLDL) remnants and plays a central role as a ligand in the receptor-mediated uptake of these particles by the liver. Here we describe a new variant of apoE, apoE1-Hammersmith, which is associated with dominantly expressed type III hyperlipidaemia. The propositus, aged 26, developed tubero-eruptive xanthomas at the age of 3, her daughter developed similar lesions at age 7 but her son, aged 3, shows no clinical abnormality so far. All three cases had an apoE3E1 phenotype and a broad beta band on lipoprotein electrophoresis. Cysteamine modification resulted in a shift of apoE1 to the apoE2 isoform position, indicating that the mutation leading to apoE1-Hammersmith occurred on an apoE3 background. ApoE genotyping confirmed these results. Sequence analysis of DNA of the propositus was performed for exons 3 and 4 and revealed a dinucleotide substitution causing two amino acid changes at adjacent positions (Lys146-->Asn) and (Arg147-->Trp).

tricor user reviews 2016-04-19

The inverse relation between coronary artery disease and the concentration of high-density lipoprotein cholesterol (HDL-C) is well established. A low HDL-C concentration is frequently accompanied by the features of the metabolic syndrome found in patients with type 2 diabetes and in individuals who are abdominally obese. Results from 3 independent trials are consistent in showing that fenofibrate is able to increase HDL-C levels across a wide range of dyslipidemic states. The HDL-C-increasing effect of fenofibrate is proportionately greater when baseline levels are low. Comparing results from published trials, the absolute increase in HDL-C produced by fenofibrate is greater than that with statins across all baseline HDL-C levels, and a 40-mg/dL treatment target HDL-C level is more likely to be achieved with fenofibrate therapy. Fenofibrate has favorable pleiotropic effects on several features of the metabolic syndrome, which are likely to explain the clinical benefits of fibrate therapy, beyond an impact on HDL-C levels. The additional reciprocal beneficial effect of fenofibrate in lowering low-density lipoprotein cholesterol (LDL-C) benefits those patients with low HDL-C and moderately increased LDL-C; the American Diabetes Association now recommends fibrate therapy in this case. Another trial, the Diabetes Atherosclerosis Intervention Study (DAIS) has also provided angiographic evidence to show that fenofibrate treatment may slow coronary artery disease progression in type 2 diabetes. Treatment effects on apolipoproteins suggest that not all fibrates affect HDL-C to an equal degree. A trial with fenofibrate focusing on coronary artery disease risk and mortality reduction in patients with type 2 diabetes that is currently under way, the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial is expected to report in 2005.