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Direct effects of fatty meals and adiposity on oxidised low-density lipoprotein.
Laguna-Camacho, A, Alonso-Barreto, AS, Mendieta-Zerón, H
Obesity research & clinical practice. 2015;(3):298-300
Abstract
High-fat intake and high adiposity contribute to hyperlipaemia. In a hyperlipaemic state, lipoproteins infiltrate arterial wall where they are modified and cause an immune response characteristic of atherosclerosis. A small fraction of modified lipoproteins including oxidised low-density lipoprotein (ox-LDL) returns to circulation. The present study tracked high-fat meals during four weeks as to find effects of sustained frequency change on adiposity and ox-LDL. The findings indicated that changes in frequency of consumption of high-fat eating episodes correlated directly with changes in adiposity and ox-LDL. Hence the number of fatty meals consumed by people with overweight or obesity in few weeks could affect the atherogenic process.
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Disrupted fatty acid distribution in HDL and LDL according to apolipoprotein E allele.
Dang, TM, Conway, V, Plourde, M
Nutrition (Burbank, Los Angeles County, Calif.). 2015;(6):807-12
Abstract
OBJECTIVES Omega-3 polyunsaturated fatty acid (ω-3 PUFA) metabolism seems to be disrupted in carriers of the epsilon 4 allele of apolipoprotein E (E4+). The objective of this study was to investigate whether the ω-3 PUFA distribution in the high and low density lipoproteins is APOE-genotype dependant before and after supplementation with ω-3 PUFAs. METHODS Eighty participants, aged between 20 and 35 y old were recruited and supplemented with 900 mg of eicosapentaenoic acid plus 680 mg of docosahexaenoic acid for 4 wk. Over the 4-wk intervention, blood samples were collected and HDL and LDL particles were obtained using sucrose gradient ultracentifugation. Fatty acid profiles of the HDL and LDL fractions were performed by gas chromatography. RESULTS Baseline anthropometric characteristics of participants were not significantly different between the two APOE-groups (E4+, N = 10; E4-, N = 70). At baseline, in the LDL of E4+ subjects, the ω-6/ω-3 PUFA ratio was 17% higher than E4- subjects. At week 4, the ω-6/ω-3 PUFA ratio was significantly higher in the LDL of E4+ than E4- subjects. There was a significant genotype × time interaction for 16:0 in HDL and LDL and for 18:2 ω-6 in HDL. DHA in the HDL was positively correlated to HDL-C levels pre- and postsupplementation in E4- only. CONCLUSIONS Contrary to what we anticipated, ω-3 PUFAs content? in HDL and LDL were not APOE isoform-dependant in young participants. However, young E4+ participants already had a tendency toward lower baseline-DHA levels in LDL particles as well as a more atherogenic ω-6/ω-3 PUFA ratio in LDL pre- and post-supplementation.
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HELP LDL apheresis reduces plasma pentraxin 3 in familial hypercholesterolemia.
Zanetti, M, Zenti, M, Barazzoni, R, Zardi, F, Semolic, A, Messa, MG, Mearelli, F, Russi, G, Fonda, M, Scarano, L, et al
PloS one. 2014;(7):e101290
Abstract
BACKGROUND Pentraxin 3 (PTX3), a key component of the humoral arm of innate immunity, is secreted by vascular cells in response to injury, possibly aiming at tuning arterial activation associated with vascular damage. Severe hypercholesterolemia as in familial hypercholesterolemia (FH) promotes vascular inflammation and atherosclerosis; low-density lipoprotein (LDL) apheresis is currently the treatment of choice to reduce plasma lipids in FH. HELP LDL apheresis affects pro- and antiinflammatory biomarkers, however its effects on PTX3 levels are unknown. We assessed the impact of FH and of LDL removal by HELP apheresis on PTX3. METHODS Plasma lipids, PTX3, and CRP were measured in 19 patients with FH undergoing chronic HELP LDL apheresis before and after treatment and in 20 control subjects. In the patients assessment of inflammation and oxidative stress markers included also plasma TNFα, fibrinogen and TBARS. RESULTS At baseline, FH patients had higher (p = 0.0002) plasma PTX3 than matched control subjects. In FH PTX3 correlated positively (p≤0.05) with age, gender and CRP and negatively (p = 0.01) with HELP LDL apheresis vintage. The latter association was confirmed after correction for age, gender and CRP. HELP LDL apheresis acutely reduced (p≤0.04) plasma PTX3, CRP, fibrinogen, TBARS and lipids, but not TNFα. No association was observed between mean decrease in PTX3 and in LDL cholesterol. PTX3 paralleled lipids, oxidative stress and inflammation markers in time-course study. CONCLUSION FH is associated with increased plasma PTX3, which is acutely reduced by HELP LDL apheresis independently of LDL cholesterol, as reflected by the lack of association between change in PTX3 and in LDL levels. These results, together with the finding of a negative relationship between PTX3 and duration of treatment suggest that HELP LDL apheresis may influence both acutely and chronically cardiovascular outcomes in FH by modulating PTX3.
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The association of very-low-density lipoprotein with ankle-brachial index in peritoneal dialysis patients with controlled serum low-density lipoprotein cholesterol level.
Kanda, E, Ai, M, Okazaki, M, Maeda, Y, Sasaki, S, Yoshida, M
BMC nephrology. 2013;:212
Abstract
BACKGROUND Peripheral artery disease (PAD) represents atherosclerotic disease and is a risk factor for death in peritoneal dialysis (PD) patients, who tend to show an atherogenic lipid profile. In this study, we investigated the relationship between lipid profile and ankle-brachial index (ABI) as an index of atherosclerosis in PD patients with controlled serum low-density lipoprotein (LDL) cholesterol level. METHODS Thirty-five PD patients, whose serum LDL cholesterol level was controlled at less than 120 mg/dl, were enrolled in this cross-sectional study in Japan. The proportions of cholesterol level to total cholesterol level (cholesterol proportion) in 20 lipoprotein fractions and the mean size of lipoprotein particles were measured using an improved method, namely, high-performance gel permeation chromatography. Multivariate linear regression analysis was adjusted for diabetes mellitus and cardiovascular and/or cerebrovascular diseases. RESULTS The mean (standard deviation) age was 61.6 (10.5) years; PD vintage, 38.5 (28.1) months; ABI, 1.07 (0.22). A low ABI (0.9 or lower) was observed in 7 patients (low-ABI group). The low-ABI group showed significantly higher cholesterol proportions in the chylomicron fraction and large very-low-density lipoproteins (VLDLs) (Fractions 3-5) than the high-ABI group (ABI>0.9). Adjusted multivariate linear regression analysis showed that ABI was negatively associated with serum VLDL cholesterol level (parameter estimate=-0.00566, p=0.0074); the cholesterol proportions in large VLDLs (Fraction 4, parameter estimate=-3.82, p=0.038; Fraction 5, parameter estimate=-3.62, p=0.0039) and medium VLDL (Fraction 6, parameter estimate=-3.25, p=0.014); and the size of VLDL particles (parameter estimate=-0.0352, p=0.032). CONCLUSIONS This study showed that the characteristics of VLDL particles were associated with ABI among PD patients. Lowering serum VLDL level may be an effective therapy against atherosclerosis in PD patients after the control of serum LDL cholesterol level.
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Oxidized low-density lipoprotein cholesterol and the ratio in the diagnosis and evaluation of therapeutic effect in patients with coronary artery disease.
Huang, H, Ma, R, Liu, D, Liu, C, Ma, Y, Mai, W, Dong, Y
Disease markers. 2012;(6):295-302
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Abstract
OBJECTIVE The purpose of the present study was to investigate the value of ox-LDL and oxidation ratio of LDL (ox-LDL/TC, ox-LDL/HDL-C and ox-LDL/LDL-C) in diagnosis and prognosis evaluation in CAD patients. Also, we aimed to observe the effect of statins on reducing level of ox-LDL and oxidation ratio of LDL, and explore whether statins still have similar effect on ox-LDL in a short period of therapy (within 2 weeks). METHODS Blood ox-LDL, TC, HDL-C, LDL-C, and TG were measured in cases with acute myocardial infarction (AMI, n=177), unstable angina pectoris (UAP, n=195), stable angina pectoris (SAP, n=228), normal control (n=120), and high risk control (n=140). RESULTS Mean value of ox-LDL and oxidation ratio of LDL was significantly higher in the CAD group than in the two control groups. The AUC of ROC curve of ox-LDL, ox-LDL/TC, ox-LDL/HDL-C, ox-LDL/LDL-C and apoA1/apoB were more than 0.50 (P < 0.001). Multivariate logistic regression analysis showed that age and ox-LDL/LDL-C related with short-term, while ox-LDL/LDL-C and ox-LDL/TC related with long-term prognosis (p < 0.05). Furthermore, after treatment with statins for 2 weeks, TC, LDL-C, ox-LDL, ox-LDL/TC, ox-LDL/HDL-C and ox-LDL/LDL-C decreased by 22%, 28%, 38%, 29%, 23% and 25% respectively. And the reduction of ox-LDL by statins is independent of lowering of LDL-C and TC. CONCLUSIONS Ox-LDL and oxidation ratio of LDL are closely related with AS, and they are better biomarkers for discriminating between patients with coronary artery disease and healthy subjects. In addition, statins can decrease level of ox-LDL significantly, which is independent of lowering of LDL-C and TC.
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Rye bread intake improves oxidation resistance of LDL in healthy humans.
Söderholm, PP, Alfthan, G, Tikkanen, MJ, Adlercreutz, H
Atherosclerosis. 2012;(2):583-6
Abstract
BACKGROUND Oxidatively modified LDL particles contribute to atherogenic development and therefore dietary interventions for promoting oxidation resistance of LDL are of interest. The capacity of LDL to resist oxidation can be determined ex vivo by exposing isolated LDL particles to copper ions and measuring the formation of conjugated dienes by spectrophotometry. OBJECTIVE The aim of this trial was to determine the effect of none versus high intake of rye bread on the oxidation resistance of LDL in healthy humans while otherwise on habitual diet. DESIGN Sixty-three healthy subjects excluded rye products for one week (baseline), followed by a stepwise addition of rye bread from 99 g/d during the first two weeks to 198 g/d during the following two weeks. Additionally plant sterols were incorporated into the rye bread for half of the subjects to study cholesterol-lowering. The resistance of LDL against copper-induced oxidation was determined at baseline and at the end of the rye-period by monitoring formation of conjugated dienes. RESULTS We observed a significant increase in the oxidation resistance of LDL, determined as a prolongation of the lag time (P < 0.001) and decrease in the slope of the propagation phase (P = 0.048) from baseline to the end of the rye-period without changes in vitamin E concentration. We observed no significant differences in the oxidation resistance of LDL between subjects who did or did not receive plant sterols. CONCLUSIONS Rye bread intake improved significantly the oxidation resistance of LDL. Further studies are needed to clarify the protective mechanism(s).
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Cardiovascular risk assessment with oxidised LDL measurement in postmenopausal women receiving intranasal estrogen replacement therapy.
Kurdoglu, M, Yildirim, M, Kurdoglu, Z, Erdem, A, Erdem, M, Bilgihan, A, Goktas, B
Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology. 2011;(8):551-7
Abstract
OBJECTIVE To investigate the effect of intranasal estrogen replacement therapy administered to postmenopausal women alone or in combination with progesterone on markers of cardiovascular risk. METHODS The study was conducted with 44 voluntary postmenopausal women. In group I (n = 15), the patients were treated with only intranasal estradiol (300 μg/day estradiol hemihydrate). In group II (n = 11), the patients received cyclic progesterone (200 mg/day micronized progesterone) for 12 days in each cycle in addition to continuous intranasal estradiol. Group III (n = 18) was the controls. Serum lipid profiles, oxidised low-density lipoprotein (LDL) and other markers of cardiovascular risk were assessed at baseline and at the 3rd month of the treatment. RESULTS Lipid profile, LDL apolipoprotein B, lipoprotein a, homocysteine, oxidised LDL values and oxidised LDL/LDL cholesterol ratio were not observed to change after 3 months compared to baseline values within each group (p > 0.016). In comparison to changes between the groups after the treatment, only oxidised LDL levels and oxidised LDL/LDL cholesterol ratios of group II were increased compared to control group (p < 0.05). CONCLUSIONS Intranasal estradiol alone did not appear to have an effect on markers of cardiovascular risk in healthy postmenopausal women. However, the addition of cyclic oral micronized progesterone to intranasal estradiol influenced the markers of cardiovascular risk negatively in comparison to non-users in healthy postmenopausal women.
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Circulating oxidized low-density lipoproteins and arterial elasticity: comparison between men with metabolic syndrome and physically active counterparts.
Pohjantähti-Maaroos, H, Palomäki, A, Kankkunen, P, Laitinen, R, Husgafvel, S, Oksanen, K
Cardiovascular diabetology. 2010;:41
Abstract
BACKGROUND Accumulation of oxidized low-density lipoproteins in the intimae of arteries and endothelial dysfunction are key events in the development of atherosclerosis. Patients with metabolic syndrome are at high risk for cardiovascular diseases but the linkage between metabolic syndrome and atherosclerosis is incompletely understood. We studied whether the levels of oxidized LDL and arterial elasticity differ between metabolic syndrome patients and physically active controls. METHODS 40 men with metabolic syndrome and 40 physically active controls participated in this cross-sectional study. None of the study subjects had been diagnosed with cardiovascular disease. Levels of oxidized LDL were assessed by a two-site ELISA immunoassay. Arterial elasticity was assessed non-invasively by the HDI/PulseWave CR-2000 arterial tonometer. RESULTS Levels of oxidized LDL were 89.6 +/- 33.1 U/L for metabolic syndrome subjects and 68.5 +/- 23.6 U/L for controls (p = 0.007). The difference remained significant after adjustment for LDL cholesterol. Large artery elasticity index (C1) was 16.2 +/- 4.1 mL/mmHgx10 for metabolic syndrome subjects and 19.4 +/- 3.7 mL/mmHgx10 for controls (p = 0.001), small artery indices (C2) were 7.0 +/- 3.2 mL/mmHgx100 and 6.5 +/- 2.9 mL/mmHgx100 (NS), respectively. CONCLUSIONS Subjects with metabolic syndrome had elevated levels of oxidized LDL and reduced large arterial elasticity compared to controls. This finding may partly explain the increased risk for cardiovascular diseases among metabolic syndrome patients. TRIAL REGISTRATION ClinicalTrials.gov NCT01114763.
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Methionine-loading rapidly impairs endothelial function, by mechanisms independent of endothelin-1: evidence for an association of fasting total homocysteine with plasma endothelin-1 levels.
Tousoulis, D, Antoniades, C, Marinou, K, Vasiliadou, C, Bouras, G, Stefanadi, E, Latsios, G, Siasos, G, Toutouzas, K, Stefanadis, C
Journal of the American College of Nutrition. 2008;(3):379-86
Abstract
OBJECTIVE Homocysteinemia is associated with elevated oxidative stress and impaired endothelial function. In the present study we examined the impact of oxidative stress in the development of endothelial dysfunction in both chronic and acute (methionine-induced) homocysteinemia in humans. We also examined the role of endothelin-1 (ET-1) in the development of endothelial dysfunction in these two conditions. METHODS In this double-blind placebo controlled study, 28 subjects of both genders (14 with homocysteinemia and 14 healthy controls) underwent methionine-loading (100mg/Kg body weight) in a standard juice, containing vitamins C (2g) plus E (800IU) (n = 14) or no vitamins (placebo group, n = 14). Forearm vasodilatory response to reactive hyperemia, plasma total homocysteine (tHcy), oxidized LDL (ox-LDL), ET-1 and soluble vascular cell adhesion molecule (sVCAM-1), were evaluated at baseline and 4 hours post methionine loading (4hPML). RESULTS Chronic homocysteinemia was associated with increased oxLDL (p < 0.01), higher ET-1 (p < 0.05) and impaired endothelial function (p < 0.01). However, oxLDL (but not ET-1) was increased 4hPML in the placebo group, an effect prevented by antioxidant vitamins. The development of severe endothelial dysfunction 4hPML was not however prevented by antioxidants. In linear regression analysis, fasting tHcy was an independent predictor of baseline oxLDL (p = 0.0001), but not of ET-1 levels. On the contrary, oxLDL was the main predictor of ET-1 (p = 0.008), suggesting that tHcy may increase ET-1 by enhancing the production of oxLDL. CONCLUSIONS Both chronic and acute methionine-induced homocysteinemia are associated with elevated oxidative stress status. Although ET-1 is increased in chronic homocysteinemia, it does not participate in the rapid development of endothelial dysfunction after methionine loading. These findings suggest that despite its potential role in chronic homocysteinemia, ET-1 has a limited contribution to the development of endothelial dysfunction in acute, methionine-induced homocysteinemia in humans.
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Serum lipid profile on admission for ischemic stroke: failure to meet National Cholesterol Education Program Adult Treatment Panel (NCEP-ATPIII) guidelines.
Smith, EE, Abdullah, AR, Amirfarzan, H, Schwamm, LH
Neurology. 2007;(9):660-5
Abstract
OBJECTIVE To determine the characteristics of patients with stroke/TIA whose admission low-density lipoprotein (LDL) levels were above goals defined by National Cholesterol Education Program Adult Treatment Panel (NCEP-ATPIII) guidelines. METHODS From January 1, 2003, to June 30, 2005, there were 1,212 discharges (1,033 stroke, 179 TIA), of whom 1,040/1,212 (86%) had lipid measurement. The preadmission individual LDL goal was determined using 2001 NCEP-ATPIII guidelines. RESULTS There were 284/1,040 (27%) whose measured LDL was greater than the individual preadmission LDL goal. Failure to be at goal was common even among those with previously diagnosed dyslipidemia (159/527, 30%) and those taking lipid-lowering agents (LLA) (71/370, 19%). LLA would have been indicated in 121/213 (57%) of those above LDL goal who were not already taking LLA, with optional consideration in 77/213 (36%). Lower LDL therapeutic targets were the strongest predictor, in a multivariable model, of failure to be at goal. Compared to LDL target <160 (reference), the OR for LDL target <130 was 6.4 (95% CI 3.4 to 12.0, p < 0.0001) and for LDL target <100 was 26.2 (95% CI 13.3 to 51.5, p < 0.0001). An increased likelihood of being at goal was associated with preadmission LLA (OR 4.2, 95% CI 2.9 to 6.2, p < 0.0001) and increasing calendar time (OR 1.09 per 3-month period, 95% CI 1.03 to 1.15, p = 0.004). CONCLUSIONS Many patients hospitalized with ischemic stroke/TIA, including those with known dyslipidemia and those taking lipid lowering agents, have measured low-density lipoprotein (LDL) that is higher than recommended by national guidelines. Patients at the greatest risk of cardiovascular events are the least likely to be at guideline-recommended LDL levels.