Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bezafibrate”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1989

Therapeutic effects of bezafibrate and gemfibrozil in hyperlipoproteinaemia type IIa and IIb.

Fifty-nine patients with hyperlipoproteinaemia Type IIa and IIb who had failed to respond to 1-month's dietary therapy were treated over a 4-month period with either bezafibrate (600 mg/day) or gemfibrozil (1200 mg/day) in addition to their diet. Fasting serum lipid (cholesterol, HDL-cholesterol and triglycerides) and blood glucose levels were measured on entry and at monthly intervals, and routine laboratory investigations were carried out before and after treatment to monitor hepatic, renal and haematic tolerance. The results showed that whilst both drugs produced significant reductions from baseline in total cholesterol, LDL-cholesterol and triglyceride levels from Day 30 onwards, the reductions were more marked in the bezafibrate group. There was a trend for HDL-cholesterol levels to increase. Fasting blood glucose levels decreased significantly in the bezafibrate group and to a greater extent than in patients on gemfibrozil. Only 1 patient on bezafibrate did not tolerate bezafibrate whereas 13 patients on gemfibrozil reported side-effects, mainly gastro-intestinal, and 4 had to withdraw from the study during the first or second month.

Adult↗
PubMed2005

Dual and pan-peroxisome proliferator-activated receptors (PPAR) co-agonism: the bezafibrate lessons.

There are three peroxisome proliferator-activated receptors (PPARs) subtypes which are commonly designated PPAR alpha, PPAR gamma and PPAR beta/delta. PPAR alpha activation increases high density lipoprotein (HDL) cholesterol synthesis, stimulates "reverse" cholesterol transport and reduces triglycerides. PPAR gamma activation results in insulin sensitization and antidiabetic action. Until recently, the biological role of PPAR beta/delta remained unclear. However, treatment of obese animals by specific PPAR delta agonists results in normalization of metabolic parameters and reduction of adiposity. Combined treatments with PPAR gamma and alpha agonists may potentially improve insulin resistance and alleviate atherogenic dyslipidemia, whereas PPAR delta properties may prevent the development of overweight which typically accompanies "pure" PPAR gamma ligands. The new generation of dual-action PPARs--the glitazars, which target PPAR-gamma and PPAR-alpha (like muraglitazar and tesaglitazar) are on deck in late-stage clinical trials and may be effective in reducing cardiovascular risk, but their long-term clinical effects are still unknown. A number of glitazars have presented problems at a late stage of clinical trials because of serious side-effects (including ragaglitazar and farglitazar). The old and well known lipid-lowering fibric acid derivative bezafibrate is the first clinically tested pan--(alpha, beta/delta, gamma) PPAR activator. It is the only pan-PPAR activator with more than a quarter of a century of therapeutic experience with a good safety profile. Therefore, bezafibrate could be considered (indeed, as a "post hoc" understanding) as an "archetype" of a clinically tested pan-PPAR ligand. Bezafibrate leads to considerable raising of HDL cholesterol and reduces triglycerides, improves insulin sensitivity and reduces blood glucose level, significantly lowering the incidence of cardiovascular events and new diabetes in patients with features of metabolic syndrome. Clinical evidences obtained from bezafibrate-based studies strongly support the concept of pan-PPAR therapeutic approach to conditions which comprise the metabolic syndrome. However, from a biochemical point of view, bezafibrate is a PPAR ligand with a relatively low potency. More powerful new compounds with pan-PPAR activity and proven long-term safety should be highly effective in a clinical setting of patients with coexisting relevant lipid and glucose metabolism disorders.

Bezafibrate↗
PubMed2003

Decreased PLTP mass but elevated PLTP activity linked to insulin resistance in HTG: effects of bezafibrate therapy.

Hypertriglyceridemia (HTG) is associated with insulin resistance, increased cholesteryl ester transfer (CET), and low HDL cholesterol. Phospholipid transfer protein (PLTP) may be involved in these relationships. Associations between CET, lipids, insulin resistance, CETP and PLTP activities, and PLTP mass were investigated in 18 HTG patients and 20 controls. Effects of 6 weeks of bezafibrate treatment were studied in HTG patients. HTG patients had higher serum triglycerides, insulin resistance, free fatty acid (FFA), and CET, lower levels of HDL cholesterol (-44%) and PLTP mass (-54%), and higher CETP (+20%) and PLTP activity (+48%) than controls. Bezafibrate reduced triglycerides, CET (-37%), insulin resistance (-53%), FFA (-48%), CETP activity (-12%), PLTP activity (-8%), and increased HDL cholesterol (+27%), whereas PLTP mass remained unchanged. Regression analysis showed a positive contribution of PLTP mass (P = 0.001) but not of PLTP activity to HDL cholesterol, whereas insulin resistance positively contributed to PLTP activity (P < 0.01). Bezafibrate-induced change in CET and HDL cholesterol correlated with changes in CETP activity and FFAs, but not with change in PLTP activity. Bezafibrate-induced change in PLTP activity correlated with change in FFAs (r = 0.455, P = 0.058). We propose that elevated PLTP activity in HTG is related to insulin resistance and not to increased PLTP mass. Bezafibrate-induced diminished insulin resistance is associated with a reduction of CET and PLTP activity.

Adrenergic beta-Antagonists↗
PubMed1989

The comparative pharmacokinetics and gastric toxicity of bezafibrate and ciprofibrate in the rat.

1. The comparative gastric toxicology and pharmacokinetics of two phenoxyisobutyrate derivatives have been evaluated in the Fischer rat. 2. After oral administration of single daily doses for 7 days, the plasma elimination half-life for bezafibrate was rapid (t1/2 of 4-5 h) in comparison to ciprofibrate (t1/2 of 76 h). 3. The area under the plasma drug concentration versus time curve (AUC) 0-24 (micrograms.h/ml +/- SD) for bezafibrate (dose 125 mg/kg per day) was 1553 +/- 334, which was less than half the value of 3748 +/- 358 achieved by ciprofibrate (10 mg/kg per day) after 7 days. 4. Oral administration of ciprofibrate at 10 mg/kg every 48 h produced similar sustained plasma concentrations to those achieved by bezafibrate 125 mg/kg dosed every 12 h. The AUC 0-48 values (micrograms.h/ml +/- SD) achieved were 5124 +/- 450 for bezafibrate compared to 4207 +/- 240 for ciprofibrate. 5. In chronic oral multidose studies with ciprofibrate and bezafibrate, similar gastric toxicity (neuroendocrine cell hyperplasia) occurred in the rat when dose regimens were adjusted to compensate for the pharmacokinetic differences between these two drugs.

Administration, Oral↗
PubMed2000

Effect of bezafibrate treatment on the altered lipoprotein profiles in hypertriglyceridemic subjects.

The effects of bezafibrate treatment on lipoprotein metabolism were investigated in hypertriglyceridemic subjects. Bezafibrate, a fibric acid derivative, was administered at 200-400 mg/day to 8 patients with hyperlipoproteinemia (type IIb and IV) for 3-6 months. We evaluated the effects of bezafibrate on the plasma levels of total cholesterol(chol), triglyceride(TG), and apoB. In addition, the lipid and apoB contents were also analyzed in VLDL, IDL, LDL and HDL fractions before and after the treatment. It was revealed that plasma levels of chol, TG and apoB significantly decreased after the treatment, 236.3 vs 210.9,192.4 vs 90.2 (p< 0.01) and 129.8 vs 116.2 (p<0.05) mg/dl respectively. VLDL-chol, VLDL-TG and VLDL-apoB dropped from 26.5,127.6 and 11.1 mg/dl to 9.1, 49.5 and 6.7 mg/dl respectively after the treatment. Regarding qualitative alterations of VLDL, TG/apoB, chol/apoB and TG + chol/apoB ratios in VLDL were significantly reduced, indicating that the size of VLDL was diminished by the treatment. In addition, HDL-chol increased from 40.4 to 60.8 mg/dl after the treatment. Consequently LDL-chol/HDL-chol significantly decreased. In conclusion, bezafibrate administration decreased the TG, chol and apoB content in VLDL, suggesting a reduced number of VLDL. Significant rise of HDL-chol and decrease of LDL-chol/HDL-chol are additional beneficial effects following bezafibrate treatment.

Apolipoproteins B↗
PubMed2000

Effect of bezafibrate or pravastatin on serum lipid levels and albuminuria in NIDDM patients.

Lipid abnormalities in diabetic patients, particularly in those with nephropathy, may be partially due to deteriorating atherosclerosis. Therefore, strict control of the lipid metabolism in addition to glycemic control is desirable. Whether or not lipid lowering drugs prevent albuminuria in diabetic patients in the long term remains unclear. This study involved 71 NIDDM patients with hypercholesterolemia (group A: n = 37, group B: N = 34). The effect of bezafibrate (group A) or pravastatin (group B) on the cholesterol (CH) content of apolipoprotein AI, B100 containing particles or remnant-like particles (RLP) or urinary albumin excretion was studied over 4 years. The CH content in apolipoprotein B100 particles after treatment with either bezafibrate or pravastatin decreased significantly (group A: 24.7%, group B: 26.6%). The CH content in RLP after treatment with bezafibrate showed a significant decrease (67.9%). Apolipoprotein AI after treatment with bezafibrate showed a significant increase (10.9%). Apolipoprotein B100 after treatment with either drug decreased significantly (group A: 19.8%, group B: 23.4%). The urinary albumin excretion rate after treatment with either drug showed no significant change over 4 years. Bezafibrate and pravastatin appear to be useful in the preventive treatment of albuminuria as well as in lowering lipid levels in NIDDM patients.

Albuminuria↗
PubMed1999

Bezafibrate, an anti-hypertriglyceridemic drug, attenuates vascular hyperresponsiveness and elevated blood pressure in fructose-induced hypertensive rats.

A high fructose diet induces hypertension, hyperinsulinemia - insulin resistance, and hypertriglyceridemia (syndrome X). In this study, we investigated the role of an abnormal lipid profile in mediating fructose-induced hypertension. We hypothesized that bezafibrate, a lipid-lowering drug, would reduce elevated blood pressure and inhibit increased vascular reactivity in fructose-fed rats. Male rats were placed on four different diets: group 1 was fed standard chow (n = 6); group 2 was fed 60% fructose (n = 5); group 3 was fed fructose plus bezafibrate (30 mg x kg(-1) x day(-1); drinking water; n = 5); and group 4 was fed standard chow plus bezafibrate (n = 6). In addition, the direct effects of very low density lipoprotein (VLDL) on vascular reactivity were examined. Bezafibrate treatment lowered blood pressure, free fatty acids, and triglycerides in the fructose-fed group, suggesting that lipid abnormalities play a role in the elevation of blood pressure in the fructose-induced hypertensive rat. Aortae from fructose-fed rats were hyperresponsive to the calcium channel agonist Bay K 8644, which was normalized with bezafibrate treatment. Incubation of aortae in a VLDL medium resulted in increased responsiveness to Bay K 8644, lending further support to lipid abnormalities altering vascular reactivity. An altered lipid profile evidenced by elevated triglycerides and free fatty acids is causally related to the development of high blood pressure and increased vascular reactivity in the fructose-induced hypertensive rat.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2000

[Marked creatine-phosphokinase elevation in myopathy after treatment with bezafibrate].

Bezafibrate is a fibric acid derivative which has been widely used in the past 15 years. Recent studies have elucidated much of its mechanism of action, which mainly results in reduction of VLDL and triglyceride levels and in elevation of HDL. The drug is relatively safe and its side-effects well known, mild, and reversible. The most severe side-effect is myositis, varying from mild flu-like symptoms to rhabdomyolysis, which is extremely rare. The underlying situations most frequently associated with bezafibrate-induced myositis are renal insufficiency and concomitant treatment with certain other drugs. We describe 2 women who developed severe myositis with bezafibrate treatment. 1, aged 43, who had moderate diabetes but no renal insufficiency, was treated with metformin and warfarin, which can interact with bezafibrate and affect its metabolism. The other, aged 54, had renal insufficiency and was on home peritoneal dialysis. Her bezafibrate dose had been increased because of very high triglyceride levels. The aim of the study is to call attention to this significant side-effect of benzafibrate and to ways of preventing it.

Adult↗
PubMedDate not supplied

Follow-up CT findings of tamoxifen-induced non-alcoholic steatohepatitis (NASH) of breast cancer patients treated with bezafibrate.

One-third of the breast cancer patients who underwent tamoxifen intake showed less than 0.9 of their liver/spleen CT (computed tomography) ratio on their annual CT study, and were diagnosed as having fatty liver (hepatic steatosis). Among them, patients who showed a lower liver/spleen CT ratio of less than 0.5 were recommended to undergo needle biopsy of the liver in order to obtain histopathological confirmation of non-alcoholic steatohepatitis (NASH), with 15 patients undergoing needle biopsy of the liver. As a result, 14 out of the 15 patients were diagnosed as having NASH, and these patients were additionally administered bezafibrate in order to prevent possible progressive changes of NASH into liver cirrhosis. In this study, we show the changes of follow-up CT findings of 6 patients with histopathologically-proven NASH who continued to undergo bezafibrate intake after the diagnosis of NASH. Two patients showed almost complete improvement as indicated by the liver/spleen CT ratio several months after completion of a tamoxifen intake of 5 years, and another 3 showed partial improvement on their liver/spleen CT ratio by bezafibrate intake in spite of continuing tamoxifen intake. Another patient with diabetes mellitus (type II) showed a continually decreasing liver/spleen CT ratio during adjuvant tamoxifen in spite of bezafibrate intake. Therefore, we concluded that the progression of NASH could be prevented by bezafibrate without any interruption of adjuvant tamoxifen treatment. For patients with diabetes mellitus, critical follow-up using CT study and laboratory tests is considered essential.

Adult↗
PubMed1992

Efficacy, safety and tolerability of lovastatin and bezafibrate retard in patients with hypercholesterolemia.

Hyperlipidemia has turned out to be the most important risk factor for coronary heart disease and necessitates frequently lipid lowering long-term treatment. Therefore, efficacy and tolerability of hypolipemic drugs are of great interest. The objective of the present study was to compare the safety, tolerability and effect on plasma lipids of Lovastatin and Bezafibrate retard in patients with hypercholesterolemia. 99 patients with total cholesterol of > or = 250 mg/dl after a 4 week standard lipid-lowering diet were treated another 4 weeks with placebo and then randomized to 400 mg Bezafibrate retard or 20 to 80 mg Lovastatin given once a day for 12 weeks. Mean changes from baseline in total cholesterol, LDL cholesterol and triglycerides were significantly reduced, in HDL cholesterol increased in both treatment-groups (p < or = 0.01). The effects of Lovastatin on total cholesterol and LDL cholesterol were more pronounced than those of Bezafibrate retard (p < or = 0.01), while Bezafibrate had a larger effect on triglycerides (p < or = 0.05). The frequency of clinical adverse experiences was low and similar among treatment groups, the frequency of laboratory adverse experiences was higher in the Lovastatin group. One patient in the Bezafibrate group was withdrawn because of nausea, one patient in the Lovastatin group because of GGT elevation.

Adult↗
PubMed1992

Effects of bezafibrate on biosynthesis of cholesterol and on degradation of native and acetylated low-density lipoproteins in incubated human monocytes.

The effects of bezafibrate on 14C-acetate incorporation into non-saponifiable lipids and on degradation of native and acetylated [125I] low-density lipoproteins (LDL) in cultured human monocytes has been evaluated. The presence of bezafibrate in the incubation medium resulted in a decrease of labelled acetate incorporation into non-saponifiable lipids. In parallel with the decrease in sterol synthesis, bezafibrate produced an increase in total and specific degradation of native low-density lipoproteins, whereas the degradation of acetylated low-density lipoproteins was not affected by the drug. These data, though obtained with concentrations of bezafibrate in the incubation medium greater than those encountered in ordinary therapeutic conditions, support the hypothesis that bezafibrate inhibits cholesterol biosynthesis and increases removal of low-density lipoproteins by activating the specific receptor pathway.

Bezafibrate↗
PubMed2005

[A case report of acute neuromyopathy induced by concomitant use of colchicine and bezafibrate].

We report a patient of acute neuromyopathy induced by concomitant use of colchicine and bezafibrate. A 75-year-old man with chronic renal failure and hyperlipidemia treated with bezafibrate (400 mg/day) for 1.5 years had developed watery diarrhea followed by acute tetraparesis, 14 days after the administration of colchicine for recurrent gout. Neurological examination showed proximal muscle weakness with myalgia, distal mild numbness (dysesthesia) of four limbs and generalized decreased or absent reflexies. The findings including elevated serum muscle enzymes, myogenic patterns with widespread myotonic discharge on the electromyography and delayed latency of F-wave on nerve conduction study indicated that the patient's clinical features were consistent with neuromyopathy. Soon after both colchicine and bezafibrate were stopped, the patient's symptoms resolved rapidly, therefore we made a diagnosis of drug-induced neuromyopathy, although rhabdomyolysis with Guillain-Barré syndrome was initially suspected. Recently, there had been reported acute and severe neuromuscular disorder induced by combination therapy with colchicine and anti-hyperlipidemic drugs, and there were clinical similarities between the cases of these reports and our case. Co-administration of colchicine with bezafibrate might accelerate the onset of neuromyopathy in connection with chronic renal failure in this case. Extreme caution is warranted when the patient with renal insufficiency concomitant use of colchicine and bezafibrate.

Acute Disease↗
PubMed1991

[Comparison about the efficacy and tolerability between simvastatin and bezafibrate in the treatment of hypercholesterolemia].

Simvastatin and bezafibrate actions on blood lipids and their side effects were compared in a double-blind trial involving 24 adults with severe type IIa or IIb primary hypercholesterolemia (mean plasma cholesterol = 4.35 g/l). During a 12-week period, the patients received either bezafibrate, 600 mg 3 times a day, or simvastatin, 10 or 20 mg once a day, with a doubling of the dosage at week 6 if the LDL-cholesterol level remained above 1.40 g/l. Simvastatin significantly reduced LDL-cholesterol by -39.5% (p less than 0.001), total cholesterol by 33.9% (p less than 0.005) and apoprotein B by -28% (p less than 0.001). Bezafibrate significantly reduced LDL-cholesterol (-19.8%, p less than 0.001) and total cholesterol (-17.5%, p less than 0.002), but not apoprotein B. Bezafibrate also reduced triglycerides by -26.6% and raised HDL-cholesterol by +27.6%. Simvastatin was more effective than bezafibrate in lowering LDL-cholesterol (p less than 0.002), total cholesterol (p less than 0.005) and apoprotein B (p less than 0.05). Tolerance of both drugs was considered excellent.

Adult↗
PubMed1991

Effect of bezafibrate & nicotinic acid on triton induced hyperlipidemias in CFY rats.

The two mechanisms of action of bezafibrate and nicotinic acid and their combination were evaluated in normal rats and triton treated rats. Bezafibrate was effective hypolipidemic agent in normal rats, but addition of nicotinic acid has certainly improved the effectiveness further which could be of clinical significance. In triton treated rats bezafibrate and nicotinic acid used individually and together had prophylactic hypolipidemic action. However, in their therapeutic effectiveness, bezafibrate reduced triglycerides (65.4%) and nicotinic acid, cholesterol (39.3%). But when treated together they showed marked acceleration in the removal of cholesterol as well as triglycerides. It is therefore concluded that a combination of bezafibrate and nicotinic acid may be beneficial in the treatment of hyperlipoproteinemias, both prophylactically and therapeutically.

Animals↗
PubMedDate not supplied

Effects of slow-release bezafibrate on serum lipids, lipoproteins, apolipoproteins, and postheparin lipolytic activities in patients with type IV and type V hypertriglyceridemia.

The effects of bezafibrate on serum lipids, lipoproteins, apolipoproteins, and post-heparin lipolytic activities were studied in 17 patients with hypertriglyceridemia. All patients received 400 mg of slow-release (SR) bezafibrate daily for four months. In the nine patients with type IV hypertriglyceridemia, mean serum triglyceride (TG) levels decreased significantly, by 53% (P less than 0.01) at two months and 50% (P less than 0.001) after four months of bezafibrate, while in the eight patients with type V, the levels decreased by 61% (P less than 0.001) and 51% (P less than 0.001), respectively. Total cholesterol levels decreased significantly (P less than 0.05) in type V patients at two and four months, by 19% and 18%, respectively, while low-density lipoprotein cholesterol levels increased significantly (P less than 0.05) in type IV patients at two and four months, by 63% and 62%, respectively. High-density lipoprotein (HDL) levels increased significantly (P less than 0.05) at two months in both patient groups. HDL subfraction analysis showed a significant (P less than 0.05) rise in HDL3-cholesterol levels in type V but not in type IV patients. Apolipoprotein (apo) A-I, A-II, and B levels increased, while apo C-II, C-III, and E levels decreased in both groups. The apo A-I/apo A-II ratio decreased significantly (P less than 0.05) at two and four months in type V patients, which also supports increased HDL3 fractions in that group. Lipoprotein lipase and hepatic TG lipase levels tended to rise, and the particle size of TG-rich lipoprotein (TGRL) and the TGRL-apo C-III/TGRL-apo C-II ratio decreased in both patient groups. These data indicate that bezafibrate-induced changes in lipoprotein profiles differed slightly in type IV and type V patients. The results confirm the usefulness of bezafibrate as a lipid-lowering agent.

Adult↗
PubMed1986

Biliary lipid secretion in patients with heterozygous familial hypercholesterolemia and combined hyperlipidemia. Influence of bezafibrate and fenofibrate.

Serum and biliary lipid metabolism were examined in 13 patients with different types of hyperlipoproteinemia before and after 4 weeks of treatment with either bezafibrate or fenofibrate. In patients with heterozygous familial hypercholesterolemia (FH), bezafibrate (n = 5) and fenofibrate (n = 7) produced a similar significant reduction of total cholesterol, LDL-cholesterol, and triglycerides by 21, 23, and 32%, respectively. In patients with familial combined hyperlipidemia (CHL), only triglycerides decreased markedly. Biliary lipid secretion rates in patients with heterozygous FH were not different from those of young male volunteers, indicating that a reduction of hepatic LDL receptors did not affect hepatic elimination of cholesterol or bile acids. Biliary cholesterol secretion increased significantly from 57 to 75 mg/hr during bezafibrate therapy (n = 8) and from 62 to 71 mg/hr during fenofibrate therapy (n = 9). No consistent change in bile acid or phospholipid secretion was observed. The elevated output of biliary cholesterol increased cholesterol saturation significantly from 147 to 185% and from 152 to 173% during administration of bezafibrate and fenofibrate, respectively. The present study indicates that treatment with bezafibrate or fenofibrate is effective in lowering LDL cholesterol in patients with heterozygous FH, but both drugs increase cholesterol saturation of bile, which might enhance the risk of cholesterol gallstone formation.

Adult↗
PubMed1995

Combined bezafibrate and simvastatin treatment for mixed hyperlipidaemia.

The safety and efficacy of combined bezafibrate-simvastatin therapy was evaluated in 49 patients with diet-resistant mixed hyperlipidaemia (type IIb). After a two-month placebo phase, patients were randomized to receive either Bezafibrate Slow Release (SR) 400 mg mane or simvastatin 20 mg nocte followed by three months combination therapy. Total cholesterol, triglycerides and high-density lipoprotein (HDL) cholesterol were measured at monthly intervals. Apolipoproteins (apo) A1 and B, lipoprotein (a) [Lp(a)] and fibrinogen were measured before and after each treatment. Simvastatin was more effective than Bezafibrate SR in reducing total cholesterol (2.0 vs. 1.1 mmol/l, p = 0.003) and lowering LDL cholesterol (1.7 vs. 0.4 mmol/l, p = 0.0001) whereas Bezafibrate SR was more effective in reducing triglycerides (by 41% vs. 17%, p = 0.001) and fibrinogen (by 23% vs. 3%, p = 0.004). Compared with simvastatin monotherapy, combined drug therapy induced further reductions in triglycerides (by 26%, p = 0.0003) and apoB (by 11 mg/dl, p = 0.03) and an increase in apoA1 (by 21 mg/dl, p = 0.0008). Symptomatic and biochemical adverse events did not occur more frequently on combined drug therapy than on monotherapy. The combination of bezafibrate and simvastatin was more effective in controlling mixed hyperlipidaemia than either drug alone and did not provoke more adverse events.

Adolescent↗
PubMed1994

Effects of treatment with bezafibrate on lipoprotein lipase activity and mass in patients with hypertriglyceridemia.

The activity and mass of lipoprotein lipase (LPL) in postheparin plasma (PHP) from patients with hypertriglyceridemia coupled with hypertension, impaired glucose tolerance, hyperinsulinemia were investigated in order to clarify the cause of hypertriglyceridemia and the effects of bezafibrate (CAS 41859-67-0), a novel lipid lowering agent. Eight weeks of treatment with bezafibrate (200 mg/d) lowered plasma total cholesterol and triglyceride by 7 and 39%, respectively, and increased plasma high density lipoprotein (HDL) cholesterol by 23% in the patients (n = 15). The LPL activity and mass of PHP in the patients were found to be lower than in the normal controls. The LPL activity and mass of PHP in the patients before treatment with bezafibrate (n = 15) were 2.05 +/- 1.06 mumol/ml/h and 147 +/- 45 ng/ml, respectively, whereas after treatment with 200 mg/d of bezafibrate for 8 weeks, these values were 3.62 +/- 1.30 mumol/ml/h (p < 0.01) and 226 +/- 57 ng/ml (p < 0.05), respectively. The increases of LPL mass were positively correlated with the decrease of triglyceride levels during the same period. These results suggest that the expression of LPL enzyme protein is impaired in patients with hypertriglyceridemia coupled with hypertension, impaired glucose tolerance and hyperinsulinemia, and the impaired expression of LPL recovers during treatment with bezafibrate, resulting in improvement of hypertriglyceridemia.

Adult↗