Effect of increasing doses of micronized fenofibrate on post-prandial triglycerides and fasting plasma lipids and lipoproteins in hypertriglyceridemic patients
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Fenofibrate
Post-prandial
Rabbits with hereditary postprandial hypertriglyceridemia exhibit central obesity and are regarded as a reliable model for metabolic syndrome. This study was performed to gain insight into the affected process of lipid metabolism and into the causative genes of the postprandial hypertriglyceridemia rabbits. Eleven genes that play key roles in lipid metabolism were selected, their mRNA levels were assessed by quantitative PCR, and their expressions were compared among postprandial hypertriglyceridemia rabbits using Japanese white rabbits as the control. Two genes appeared to be in causal connection with postprandial hypertriglyceridemia, and these were regarded as likely candidates for the pathogenesis. One was the fatty acid synthase gene, which had an expression constitutively higher in postprandial hypertriglyceridemia rabbits than in Japanese white rabbits during the fasting state and reached quite high levels after feeding. The other was the gene for hepatic triglyceride lipase with an expression that was approximately one order lower than that found in the Japanese white rabbits. The low plasma hepatic triglyceride lipase activities were consistent with the low levels of the transcript in the livers of the postprandial hypertriglyceridemia rabbits. Thus, elevated fatty acid synthesis and defected lipid hydrolysis together would cause the postprandial hypertriglyceridemia in postprandial hypertriglyceridemia rabbits.
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Background: Omega-3 fatty acids and fenofibrate are both used to treat patients with hypertriglyceridemia. However, a head-to-head comparison of the lipoprotein and metabolic effects of these two medicines has not been published. Methods: This was a randomized, single-blind, placebo-controlled, parallel study. Age, sex, and body mass index were matched among groups. All patients were recommended to maintain a low fat diet. Fifty patients in each group were given placebo, omega-3 fatty acids 2 g (most commonly used dosage in Korean patients), or fenofibrate 160 mg, respectively daily for 2 months. Results: Omega-3 fatty acids therapy decreased triglycerides by 21% and triglycerides/HDL cholesterol and improved flow-mediated dilation (P<0.01)), however, did not significantly change insulin, plasma adiponectin levels, and insulin sensitivity (determined by QUICKI) relative to baseline measurements. Fenofibrate therapy decreased total cholesterol, triglycerides by 29%, and triglycerides/HDL-cholesterol (all P<0.01) and improved flow-mediated dilation when compared with baseline. When compared with placebo and omega-3 fatty acids, fenofibrate therapy decreased non-HDL cholesterol (P<0.001) and triglycerides/HDL cholesterol (P=0.016) while increasing HDL cholesterol (P<0.001) and apolipoprotein AI (P=0.001). Of note, when compared with omega-3 fatty acids, fenofibrate therapy decreased fasting insulin (P=0.023) and increased plasma adiponectin (P=0.002) and insulin sensitivity (P=0.015). Conclusions: Omega-3 fatty acids and fenofibrate therapy promoted similar changes in triglycerides and endothelium-dependent dilation. However, fenofibrate therapy had substantially better effects on lipoprotein and metabolic profiles in patients with hypertriglyceridemia.
Fenofibrate
Clofibrate
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Human immunodeficiency virus (HIV) protease inhibitors are associated with several metabolic abnormalities including hypercholesterolemia and hypertriglyceridemia. Fenofibrate is a new lipid-lowering agent for adults with very high triglyceride levels that was administered to two HIV-positive patients who were taking protease inhibitors and developed hypertriglyceridemia. Starting dosages were 134 and 201 mg/day, and were increased to 268 mg/day in both patients. Triglyceride levels decreased from 1450 to 337 mg/dl (76.8%) and from 1985 to 322 mg/dl (83.8%), respectively, after 10 months of therapy. High-density lipoprotein levels increased in both patients.
Fenofibrate
Protease inhibitor (pharmacology)
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To explore the clinical implications of postprandial hypertriglyceridemia in postmenopausal Japanese women.Postprandial blood samples were collected from 91 women at their initial visit, with fasting blood samples collected within the following month to examine their lipid profiles. These women were grouped into normotriglyceridemia (fasting/postprandial triglycerides [TG] < 150; n = 36), mild postprandial hypertriglyceridemia (fasting TG < 150, postprandial TG > or = 150, < 225; n = 27), moderate postprandial hypertriglyceridemia (fasting TG < 150, postprandial TG > or = 225; n = 19) and hypertriglyceridemia (fasting TG > or = 150; n = 9) by using 225 mg/dL as the cut-off value for postprandial hypertriglyceridemia.The subjects were 54.1 +/- 7.8 years old; their duration of menopause, 6.0 +/- 7.7 years; body mass index, 21.4 +/- 4.0 kg/m(2); postprandial TG concentration, 189 +/- 110 mg/dL; and fasting TG concentration, 109 +/- 50 mg/dL. Approximately 50% (n = 46) of the women had normal fasting TG (fasting TG < 150), but high postprandial TG (postprandial TG > or = 150). Approximately 10% (n = 9) of the women had hypertriglyceridemia (fasting TG > or = 150 mg/dL). In those with postprandial hypertriglyceridemia (n = 46), postprandial TG negatively correlated with high-density lipoprotein cholesterol (HDL-C), while fasting TG showed no such correlation with HDL-C.Postprandial TG may provide a better understanding of lipid metabolism in postmenopausal women.
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Fasting and postprandial hypertriglyceridemia are causal risk factors for atherosclerosis. The prevalence of hypertriglyceridemia is approximately 25–30% and most hypertriglyceridemic patients suffer from mild to moderate hypertriglyceridemia. Data regarding dietary interventions on postprandial triglyceride metabolism of mildly to moderately hypertriglyceridemic patients is, however, sparse. In a randomized controlled trial, eight mildly hypertriglyceridemic patients and five healthy, normolipidemic controls received three separate standardized fat-meals containing either saturated fatty acids (SFA), mono-unsaturated fatty acids (MUFA), or medium-chain fatty acids (MCFA) in a randomized order. Fasting and postprandial lipid parameters were determined over a 10 h period and the (incremental) area under the curve (AUC/iAUC) for plasma triglycerides and other parameters were determined. MCFA do not lead to a significant elevation of postprandial total plasma triglycerides and other triglyceride parameters, while both SFA (patients: p = 0.003, controls: p = 0.03 compared to MCFA) and MUFA (patients: p = 0.001; controls: p = 0.14 compared to MCFA) do lead to such an increase. Patients experienced a significantly more pronounced increase of plasma triglycerides than controls (SFA: patients iAUC = 1006 mg*h/dL, controls iAUC = 247 mg*h/dL, p = 0.02; MUFA: patients iAUC = 962 mg*h/dL, controls iAUC = 248 mg*h/dL, p = 0.05). Replacing SFA with MCFA may be a treatment option for mildly to moderately hypertriglyceridemic patients as it prevents postprandial hypertriglyceridemia.
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Objectives To investigate endothelium-dependent flow-mediated dilatation(FMD) and the serum level of matrix metalloproteinase-2 (MMP-2) in hypertriglyceridemia patients and to study effect of fenofibrate. Methods FMD and serum concentrations of MMP-2 were determined in 30 patients with hypertriglyceridemia and 30 normal controls. Patients with hypertriglyceridemia were treated with fenofibrate. After 8 weeks, transformations of FMD and serum levels of MMP-2 were determined. Results Patients with hypertriglyceridemia caused a marked decrease in endothelium-dependent flow-mediated dilatation (FMD). Compared with control, the serum levels of MMP-2 and tumor necrosis factor-α(TNF-α) were markedly increased in patients. After treatment with fenofibrate for 8 weeks, FMD of the patients were improved. Treated with fenofibrate significantly reduced the elevated levels of MMP-2 and TNF-α. Conclusions These results suggest that patients with hypertriglyceridemia have vascular endothelium dysfunction and the management of fenofibrate can improve the patients' FMD. The protective effect of fenofibrate on endothelial cells maybe relates to reduction of serum MMP-2 level.
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Matrix metalloproteinase 9
Endothelial Dysfunction
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Introduction: Hypertriglyceridemia is known as an independent risk factor for coronary artery disease (CAD). Fenofibrate that is used for the treatment of hypertriglyceridemia can prevent cardiovascular events in patients with CAD. However, there is little information regarding the vascular effects of fenofibrate on arterial wall stiffness in patients with hypertriglyceridemia and without CAD, diabetes mellitus (DT), and hypertension (HT). The objective of this study is to evaluate the effects of fenofibrate treatment on the arterial stiffness in the patients with pure hypertriglyceridemia.
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We investigated the effects of fenofibrate on C-reactive protein (CRP) levels in patients with hypertriglyceridemia. Patients with a triglyceride level ≥200 mg/dL were randomly assigned to receive either 200 mg of fenofibrate (n=54) or general measures (n=54). A third group of patients with hypercholesterolemia received a statin (n=54). Patients with a CRP level ≥10 mg/L were excluded. CRP levels were measured before and after 2 months of therapy. Fenofibrate did not reduce CRP levels (1.74±1.74 vs. 1.54±1.66 mg/L, P=0.27) nor did general measures (P=0.85). Statin reduced CRP levels (P=0.002). In patients with baseline CRP levels of ≥3 mg/dL, CRP levels were decreased in both the fenofibrate and control groups (P=0.026 and 0.008, respectively). Changes in CRP levels were associated only with baseline CRP levels in both groups (P=0.001 and 0.049, respectively). When all hypertriglyceridemic patients were divided into 2 subgroups according to changes in body weights, CRP levels decreased in patients who reduced their body weight ≥1 kg (n=29, P=0.030), and were not changed in the other patients (n=79, P=0.67). In summary, fenofibrate failed to decrease CRP levels in patients with hypertriglyceridemia. An anti-inflammatory mechanism may not play a significant role in the cardioprotective effect of fenofibrate.
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