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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous research has linked hyperlipidemia with increased serum concentrations of lipid peroxidation products; however, a specific association between diet-induced oxidative stress and hyperlipidemia has not been studied. In the present study, the relationship between tissue lipid peroxidation and hyperlipidemia induced by ingestion of fish oil was examined. In Experiment 1, male Golden Syrian hamsters were fed semipurified diets composed of 1.6 wt% safflower oil plus 15.0 wt% of either butterfat (BF), safflower oil (SAFF), or high-cholesterol menhaden oil [MHO(H-CHOL)] semipurified diets for 27 d. The cholesterol contents of the diets were adjusted to 0.088%. The MHO(H-CHOL)-fed hamsters exhibited higher serum concentrations of total cholesterol, triglycerides, apolipoprotein B, and lipid peroxides when compared to the BF and SAFF diet groups. In a further study (Experiment 2), hamsters were fed for 27 d three dietary treatments: (i) MHO(H-CHOL) with no vitamin E content; (ii) a low-cholesterol menhaden oil containing high concentrations of vitamin E (2.5 mg tocopherol/g oil or dietary concentrations of 375 mg/kg) [MHO(L-CHOL) + E]; and (iii) the MHO(L-CHOL + E) with added cholesterol (595 mg/kg) [MHO(L-CHOL) + CHOL + E] to match the cholesterol content of the MHO(H-CHOL). The MHO(L-CHOL) + E and MHO(L-CHOL) + CHOL + E diet groups showed lower concentrations of serum cholesterol, triglycerides, and hepatic lipid peroxides than the MHO(H-CHOL)-treated group. Moreover, in contrast to the hypercholesterolemia caused by the MHO(H-CHOL) feeding, the MHO(L-CHOL)+ E and MHO(L-CHOL) + CHOL + E diets did not show a serum cholesterol-elevating action. This study supports the hypothesis that oxidative stress in the Syrian hamster could play a causal role in dietary-induced hyperlipidemia which can be inhibited by high vitamin E intake.
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PMID:Vitamin E inhibits fish oil-induced hyperlipidemia and tissue lipid peroxidation in hamsters. 886 86

Recently, hyperlipidemia as well as hypertension has been observed in Dahl salt-sensitive (S) rats. In this study, to investigate whether the lipid abnormality is involved in the renal injury of Dahl S rats, we examined the effect of vitamin E on glomerular sclerosis, as vitamin E is an inhibitor of lipid oxidation. Dahl S rats were given a high salt diet (8% NaCl) containing either normal vitamin E (2 mg/100 g) or high vitamin E (50 mg/100 g) for 4 weeks. Dahl salt-resistant (R) rats were given a high salt and normal vitamin E diet. The blood pressure in the Dahl rats increased and was not suppressed by the vitamin E supplement. Serum cholesterol and triglycerides in Dahl S rats were higher than in Dahl R rats at both 0 and 4 weeks. Vitamin E lowered the serum cholesterol level in Dahl S rats at 4 weeks (126 +/- 5 v 150 +/- 12 mg/dL, P < .01). Urinary protein excretion and serum creatinine increased in Dahl S rats, and vitamin E inhibited the increases significantly (urinary protein, 70.7 +/- 0.9 v 178.0 +/- 8.8 mg/day, P < .01; serum creatinine, 0.45 +/- 0.02 v 0.63 +/- 0.05 mg/dL, P < .01). Serum lipid peroxide (LPO) was higher in Dahl S rats than in Dahl R rats, and vitamin E lowered LPO in Dahl S rats (2.10 +/- 0.03 v 2.70 +/- 0.04 nmol/mL, P < .01). In the histologic study, sclerosing score (SS) of glomeruli, which represents the degree of glomerulosclerosis semiquantitatively, was higher in Dahl S rats than in Dahl R rats. Vitamin E lowered SS (114 +/- 3 v 157 +/- 6, P < .01) and ameliorated arterial injuries such as medial thickness with partial necrosis and severe fibrinoid proliferation with inflammatory cell infiltration. In all rats, SS was strongly correlated with urinary protein (r = 0.93, P < .01), serum cholesterol (r = 0.86, P < .01), and serum LPO (r = 0.89, P < .01). These results suggest that the renal injury in Dahl S rats is caused not only by hypertension but also by hyperlipidemia. Therefore, vitamin E might ameliorate the renal damage by inhibiting the oxidation of lipids.
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PMID:Vitamin E ameliorates the renal injury of Dahl salt-sensitive rats. 916 Jul 94

The present study was to investigate the levels of plasma lipid peroxide products including malondialdehyde (MDA) and conjugated dienes (CD), and antioxidants including enzyme superoxide dismutase, glutathione peroxidase, catalase, plasma vitamin E and vitamin C in diabetic patients. Fifty-eight diabetic subjects; 16 males and 42 females, aged 30-75 years, were recruited. Eighteen of them had diabetes and forty of them had diabetes with hyperlipidemia. Twenty-seven healthy subjects, 8 males and 19 females, aged 30-75 years, were used as the control group. The results showed that the concentrations of plasma MDA in diabetic patients with or without hyperlipidemia tended to be increased when compared to the controls but there were no significant differences. The CD values were increased significantly in both diabetic groups when compared with control subjects. Significantly elevated levels of plasma MDA and CD were found in diabetic patients with hypertriglyceridemia (> 150 mg%). This increment did not change the antioxidant status in both enzymes and vitamins except that the plasma vitamin E levels and the ratios of tocopherol: cholesterol were increased significantly. An increase of lipid peroxide in plasma may be one important factor in the development of vascular complication and atherosclerosis seen in diabetic patients.
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PMID:Plasma lipid peroxide and antioxidant levels in diabetic patients. 924 11

The effects of marine omega-3 polyunsaturated fatty acids (FAs) and antioxidants on the oxidative modification of LDL were studied in a randomized, double-blind, placebo-controlled trial. Male smokers (n = 41) with combined hyperlipidemia were allocated to one of four groups receiving supplementation with omega-3 FAs (5 g eicosapentaenoic acid and docosahexaenoic acid per day), antioxidants (75 mg vitamin E, 150 mg vitamin C, 15 mg beta-carotene, and 30 mg coenzyme Q10 per day), both omega-3 FAs and antioxidants, or control oils. LDL and human mononuclear cells were isolated from the patients at baseline and after 6 weeks of supplementation. LDL was subjected to cell-mediated oxidation by the patients' own mononuclear cells, as well as to Cu(2+)-catalyzed and 2,2'-azobis-(2-amidinopropane hydrochloride) (AAPH)-initiated oxidation. Extent of LDL modification was measured as lag time, the formation rate of conjugated dienes (CDs), the maximum amount of CDs formed, formation of lipid peroxides, and the relative electrophoretic mobility of LDL on agarose gels. Dietary supplementation with omega-3 FAs increased the concentration of total omega-3 FAs in LDL and reduced the concentration of vitamin E in serum. The omega-3 FA-enriched LDL particles were not more susceptible to Cu(2+)-catalyzed, AAPH-initiated, or autologous cell-mediated oxidation than control LDL. In fact, enrichment with omega-3 FAs significantly reduced the formation rate of CDs when LDL was subjected to AAPH-induced oxidation. Supplementation with moderate amounts of antioxidants significantly increased the concentration of vitamin E in serum and increased the resistance of LDL to undergo Cu(2+)-catalyzed oxidation, measured as increased lag time, reduced formation of lipid peroxides, and reduced relative electrophoretic mobility compared with control LDL. Supplementation with omega-3 FAs/antioxidants showed oxidizability of LDL similar to that of control LDL and omega-3 FA-enriched LDL. In conclusion, omega-3 FAs neither rendered the LDL particles more susceptible to undergo in vitro oxidation nor influenced mononuclear cells' ability to oxidize autologous LDL, whereas moderate amounts of antioxidants protected LDL against oxidative modification.
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PMID:Peroxidation of LDL from combined-hyperlipidemic male smokers supplied with omega-3 fatty acids and antioxidants. 940 30

Previous reports have shown that administration of fibrates can reduce coronary events and also improve plasma lipid levels. Oxidative modification of low density lipoprotein has been implicated in the pathogenesis of atherosclerosis, and the resistance of low density lipoprotein (LDL) to in vitro oxidation has been found to be correlated with the extent of atherosclerosis. We performed a double-blind, placebo-controlled intervention trial to establish whether gemfibrozil could improve resistance of LDL to oxidation in patients with hyperlipidemia. Patients were randomly assigned to treatment with gemfibrozil (450 mg, twice a day, n = 10) or placebo (n = 9) for 8 weeks. Blood samples were obtained after an overnight (12 h) fast. Gemfibrozil administration significantly reduced total plasma cholesterol and triglyceride levels and changed the LDL from small, dense particles (pattern B, < or = 25.5 nm) to larger, more buoyant particles (pattern A, > 25.5 nm). Gemfibrozil significantly increased the lag time of LDL oxidation in vitro by 18.2% from 45.5 +/- 8.0 min at week 0 to 53.4 +/- 11.4 min at week 8, but did not change LDL vitamin E and beta-carotene concentrations. Surprisingly, gemfibrozil significantly decreased LDL lipid peroxides by -33.1% and increased the LDL vitamin E/lipid peroxide ratio by 67.6% from 1.3 +/- 0.5 at week 0 to 2.1 +/- 0.9 at week 8. These results demonstrate that gemfibrozil treatment can render LDL less susceptible to oxidative modification while reducing plasma cholesterol and triglyceride and improving LDL subclass pattern. This antioxidative effect of gemfibrozil on LDL may be one of the factors which could delay the progression of atherosclerosis.
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PMID:Beneficial effect of gemfibrozil on the chemical composition and oxidative susceptibility of low density lipoprotein: a randomized, double-blind, placebo-controlled study. 969 6

Eighteen children with steroid-sensitive nephrotic syndrome (SSNS) were studied. The control group comprised 20 healthy children. The following indirect parameters of reactive oxygen species activity were determined in nephrotic patients during four stages of the disease (full relapse before prednisone administration, disappearance of proteinuria, prednisone cessation, unmaintained remission): plasma malondialdehyde (MDA) levels, copper/zinc superoxide dismutase (CuZn SOD) activity and glutathione peroxidase (GPX) activity in erythrocytes, reduced glutathione (GSH) and vitamin C levels in whole blood, and vitamin E level in serum. Increased MDA levels, reduced vitamin C levels, and enhanced CuZn SOD activity were found in relapse. GSH concentration was high during all four stages. Vitamin E level was also increased, parallel to the pattern of serum lipids. GPX activity remained low during the proteinuria stage and in remission. We conclude that the majority of abnormal findings can be attributed to the hyperlipidemia of NS. Low GPX activity may be a factor limiting the antioxidant capacity in NS. The present study is inconclusive regarding the role of free radicals in the proteinuria of NS.
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PMID:Antioxidant status of children with steroid-sensitive nephrotic syndrome. 987 20

Vitamins A and E differ in hydrophobicity. When added to a fat load more or less specific labeling of chylomicrons and their remnants can be expected and this allows to approach the mechanism of postprandial lipemia from a new sight of view. Applied in a study in which 20 patients participated (eight patients with familial dysbetalipoproteinemia (FD), six patients with familial combined hyperlipidemia (FCH) and six controls) we found that vitamin A, no longer paralleled the apo B-48 concentrations from 9 h after a fat load, especially in the remnant fraction with Sf 15-100. Qualitatively, the distribution of vitamin A to the more dense fractions mirrored that of vitamin E, but the latter was more rapid. Both vitamins at the maximum of remnant-accumulation, at 14 h after the fat load, correlated with the cholesterol content of the remnant fraction. For vitamin E there was a similar concentration dependent distribution to all other lipoprotein fractions. The results confirm our view that the lipoprotein mechanism can be regarded as a dynamic system. During regular episodes following the meals, exogenous fat is, like the vitamins, distributed over all endogenously formed lipoproteins. This transfer process results in the formation of beta-VLDL and contributes to the pathogenesis of FCH and FD.
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PMID:Fat loading experiments with the vitamins A and E suggest that in postprandial lipemia transfer/diffusion of chylomicron lipids to VLDL contributes to beta-VLDL formation. 988 53

This study analysed the diet (based on a 7-day-record), smoking habits and basic anthropometric parameters of patients with familial combined hyperlipidaemia (N = 154, 52% men, 48% women, mean age 55.73 +/- 12.95). These data were correlated with blood lipids and lipoproteins. In high-risk patients' diets we found not quantitative, but mostly qualitative shortcomings: the average energy intake was 104% of the recommended daily intake (RDI), but 34% of the energy was derived from fats. The daily fat intake represented 137% of RDI, and 60 g were of animal and 24 g of vegetable origine. The protein intake was 120% of RDI (155% animal, 75% vegetable protein), the carbohydrate intake was only 86% and the fibre intake 71% of RDI. A very high intake both of cholesterol--139% of RDI and NaCl 151% of RDI--was recorded, while the intake of antioxidant vitamins C and E was only 82% and 35% of RDI, respectively. Current smoking was recorded in 51% of patients. Smokers had also a poorer diet: higher animal fat and protein, as well as a higher cholesterol intake, lower vegetable fat, protein, fibre and vitamin E intake. Surprisingly smokers were found to ingest more vitamin C than non-smokers. As to blood lipids: smokers vs. non-smokers had the following values in mmol/l (SD): total cholesterol 7.8 (+/- 1.3) vs. 7.7 (+/- 1.82), triacylglycerols 3.27 (+/- 2.13) vs. 3.2 (+/- 3.11), HDL-cholesterol 1.25 (+/- 0.39) vs. 1.36 (+/- 0.43), LDL-cholesterol 5.11 (+/- 1.39) vs. 4.95 (+/- 1.51), and, in g/l, apolipoprotein A1 1.8 (+/- 0.30) vs. 1.66 (+/- 0.35), apolipoprotein B 1.66 (+/- 0.35) vs. 1.52 (+/- 0.44), lipoprotein (a) 0.36 (+/- 0.27) vs. 0.43 (+/- 0.50), all without statistical significance. For smokers vs. non-smokers anthropometric data were as follows (mean, SD): body mass index (BMI) 27.74 (+/- 3.77) vs. 27.02 (+/- 3.30), waist/hip ratio (WHR) 0.895 (+/- 0.086) vs. 0.911 (+/- 0.093), and % of body fat 29.6 (+/- 7.4) vs. 27.9 (+/- 7.9). Our conclusions suggest, that lifestyle choice are of great importance for patients with this serious genetic lipid metabolism disorder and that it is important to recognise the danger of risk factor cumulation in connection with cardiovascular diseases.
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PMID:Diet, smoking, and blood lipids in patients with combined familial hyperlipidaemia. 1008 16

Hyperlipidemia is a striking feature of nephrotic syndrome (NS) and the lipid profile seen in NS is accepted as atherogenic. Both low density lipoprotein (LDL) and very low density lipoprotein (VLDL) are apolipoprotein B-containing lipoproteins which are accepted as atherogenic. Oxidized-LDL (ox-LDL) has been suggested to play a fundamental role in atherogenesis. In this study, male Sprague-Dawley rats were made nephrotic by a single intraperitoneal injection of puromycin aminonucleoside (100 mg/kg body weight). We found significant elevation in serum triglycerides, total cholesterol, malondialdehyde, vitamin E levels and total cholesterol/vitamin E ratio and decrease in total protein and albumin levels in the NS group (n:8) compared with the control group (n:9). High density lipoprotein (HDL)-cholesterol and free fatty acid levels were not significantly different between these two groups. Apolipoprotein B-containing lipoproteins (non-HDL fraction) were separated by precipitation and amount of thiobarbituric acid-reactive substances (TBARS) of non-HDL fraction were measured after 60, 90, 120, 180 minutes of incubation with copper sulphate. TBARS levels of non-HDL fraction were significantly higher in the NS group compared with the control group at all of the time periods above. In nephrotic animals, the increased lipid peroxidation was influenced by serum lipids.
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PMID:Susceptibility of non-HDL fraction to oxidation in experimental nephrotic syndrome. 1040 Dec 26

n-3 Fatty acids have been shown to modify several key risk factors for cardiovascular disease. However, it is not clear whether the apparent protection against cardiovascular disease is directly related to antiatherogenic functions of these fatty acids or is mediated through their modification of the risk factors through mechanisms not directly related to lipids. A major question concerns the importance of lipid modification, which is a potent outcome of fish-oil supplementation. On balance, lipid modification is likely to represent a significant antiatherogenic factor. The benefits include increased HDL(2)-cholesterol concentrations, reduced triacylglycerol-rich lipoprotein concentrations, reduced postprandial lipemia, and reduced remnant concentrations. In contrast, LDL-cholesterol concentrations have often been noted to rise and the potential of increased oxidizability of LDLs is potentially adverse with lipid modification, but this potential can be overcome with vitamin E supplementation. The characteristic lipid changes and the underlying mechanisms are reviewed. Additional benefits of fish oils include improved endothelial function and better arterial compliance (elasticity). Future trials will be needed to determine minimum effective dosages of eicosapentaenoic and docosahexaenoic acids over lengthy periods and to show cardiovascular disease reduction through intervention.
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PMID:Fish oil and cardiovascular disease: lipids and arterial function. 1061 76


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