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The current study was designed to investigate the short-term effects of policosanol consumption on blood pressure (BP) and the lipid parameters in healthy Korean participants with prehypertension. A total of 84 healthy participants were randomly allocated to three groups receiving placebo, 10 mg of policosanol, or 20 mg of policosanol for 12 weeks. Based on an average of three measurements of peripheral BP, the policosanol 20 mg group exhibited the most significant reduction, that is, up to 7.7% reduction of average systolic BP (SBP) from 136.3 ± 6.1 mmHg (week 0) to 125.9 ± 8.6 mmHg (week 12, p < 0.001). Between group comparisons using repeated measures ANOVA showed that the policosanol 20 mg group had a significant reduction of SBP at 12 weeks ( p = 0.020) and a reduction of diastolic BP (DBP) at 8 weeks ( p = 0.041) and 12 weeks ( p = 0.035). The policosanol 10 mg and 20 mg groups showed significant reductions in aortic SBP of 7.4% and 8.3%, respectively. The policosanol groups showed significant reductions of total cholesterol (TC) of 9.6% and 8.6% and low-density lipoproteins (LDL-C) of 21% and 18% for 10 mg and 20 mg of policosanol, respectively. Between group comparisons using repeated measures ANOVA showed that the policosanol (10 mg and 20 mg) groups at 12 weeks had a significant reduction of TC ( p = 0.0004 and p = 0.001) and LDL-C ( p = 0.00005 and p = 0.0001) and elevation of %HDL-C ( p = 0.048 and p = 0.014). In conclusion, 12-week consumption of policosanol resulted in significant reductions of peripheral SBP and DBP, aortic SBP and DBP, mean arterial pressure (MAP), and serum TC and LDL-C with elevation of % HDL-C.

People who maintain ideal cardiovascular heath have a low lifetime risk of cardiovascular disease. Therefore, encouraging people to achieve ideal cardiovascular health represents an important opportunity to improve the prevention of cardiovascular disease. However, preventing cardiovascular disease by promoting ideal cardiovascular health requires shifting the focus from treating disease after it develops to preventing cardiovascular events before they happen by slowing the progression of atherosclerosis. Because atherogenic lipoproteins play a central causal role in the initiation and progression of atherosclerosis, maintaining optimal lipid levels is necessary to achieve ideal cardiovascular health. This review describes the cumulative effect of lipid-carrying lipoproteins on the risk of cardiovascular disease, estimates the magnitude of the clinical benefit that can be achieved by maintaining optimal lipid levels, identifies the most effective timing for implementing strategies designed to achieve optimal lipid levels, and provides a clinical pathway to help people achieve the lipid levels necessary for ideal cardiovascular health., (Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objective: To explore the association of asthma with serum levels of high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol, and triglyceride., Methods: PubMed, Cochrane, and Embase databases were systematically searched through November 2015 using the following search terms: dyslipidemia, HDL, LDL, triglyceride, cholesterol, and asthma. Eligible studies included randomized controlled trials (RCTs), retrospective, cohort, and cross-sectional studies. Sensitivity analysis and publication bias were performed., Results: Twenty studies were included in the analysis, with a total 32,604 patients (3,458 in the asthma group and 29,146 in the control group). The pooled analysis found that the mean difference between groups was significantly higher in the asthma group for levels of LDL (6.026 mg/dL, 95% CI = 2.696-9.356, p < .001) and total cholesterol (8.161 mg/dL, 95% CI = 3.006-13.316, p = .002) compared with the control group. No association was observed between asthma and control groups for levels of HDL (mean difference = -0.728, 95% CI = -3.146-1.691, p = .555) or triglycerides (mean difference = 1.436, 95% CI = -2.768-5.640, p = .503)., Conclusions: Levels of LDL and total cholesterol were higher in patients with asthma than non-asthmatic patients.

Background: In the Determining the Efficacy and Tolerability of cholesteryl ester transfer protein (CETP) INhibition with AnacEtrapib (DEFINE) trial, anacetrapib added to statin produced robust low-density lipoprotein cholesterol (LDL-C)-lowering and high-density lipoprotein cholesterol (HDL-C)-raising vs placebo in patients with coronary heart disease (CHD). Predictors of the degree of LDL-C and HDL-C responses to anacetrapib, however, are poorly understood., Objective: Lipid effects of anacetrapib in patient subgroups within the DEFINE trial (clinicaltrials.gov: NCT00685776) are reported., Methods: The percent of placebo-corrected changes from baseline for LDL-C (estimated by Friedewald calculation [Fc-LDL-C]) and HDL-C after 24 weeks of anacetrapib 100 mg/day were compared among patients by age, gender, race, diabetes status, type of concomitant statin with or without other lipid therapies, and baseline HDL-C, Fc-LDL-C, and triglyceride (TG) levels., Results: Percent decreases in Fc-LDL-C and increases in HDL-C with anacetrapib were similar (magnitude of difference generally <1/5 of the overall treatment effect) across subgroups by age, gender, diabetes status, lipid-modifying regimen, and baseline Fc-LDL-C, HDL-C, or TG. On the other hand, anacetrapib effects on Fc-LDL-C (-24% vs -41%) and HDL-C (+75% vs +139%) appeared to be less in black vs white patients, respectively., Conclusion: Effects of anacetrapib on Fc-LDL-C and HDL-C were generally comparable across subgroups, including being relatively independent of baseline Fc-LDL-C, HDL-C, or TG levels. The clinical impact of the lipid-modifying effects of anacetrapib is being evaluated in the cardiovascular disease outcomes trial, Randomized EValuation of the Effects of Anacetrapib though Lipid-modification (REVEAL)., (Copyright © 2015 National Lipid Association. Published by Elsevier Inc. All rights reserved.)

Background Childhood cancer survivors have increased risk of dyslipidemia and atherosclerotic cardiovascular disease (CVD). The aim of this study was to evaluate the prevalence and associated cardiovascular risks of specific lipid abnormalities among childhood cancer survivors. Methods Comprehensive lipid panel measurements were obtained from 4115 5-year survivors, with 3406 (mean age at evaluation = 35.2 years, SD = 10.4 years) not having previous dyslipidemia diagnosis, as well as 624 age, sex, and race and ethnicity matched community controls. Results Previously undiagnosed dyslipidemia with abnormal low-density lipoprotein (LDL) cholesterol (>160 mg/dL), non–high density lipoprotein (HDL) cholesterol (>190 mg/dL), HDL cholesterol (<40 mg/dL for men, <50 mg/dL for women), and triglycerides (>150 mg/dL) were identified in 4%, 6%, 30%, and 17%, respectively. Survivors without previous dyslipidemia diagnosis had higher LDL cholesterol and non-HDL cholesterol and lower HDL cholesterol than community controls. Cranial radiotherapy (relative risk [RR] = 2.2, 95% confidence interval [CI] = 1.6 to 3.0 for non-HDL cholesterol) and total body irradiation for hematopoietic cell transplantation (RR = 6.7, 95% CI = 3.5 to 13.0 for non-HDL cholesterol; RR = 9.9, 95% CI = 6.0 to 16.3 for triglycerides) were associated with greater risk of dyslipidemia. Diagnoses of low HDL cholesterol (hazard ratio [HR] = 2.9, 95% CI = 1.8 to 4.7) and elevated triglycerides (HR = 3.1, 95% CI = 1.9 to 5.1) were associated with increased risk for myocardial infarction, and diagnoses of high LDL cholesterol (HR = 2.2, 95% CI = 1.3 to 3.7), high non-HDL cholesterol (HR = 2.2, 95% CI = 1.3 to 3.7), low HDL cholesterol (HR = 3.9, 95% CI = 2.8 to 5.4), and elevated triglycerides (HR = 3.8, 95% CI = 2.7 to 5.5) were associated with increased risk for cardiomyopathy. Conclusions Previously undiagnosed dyslipidemia among childhood cancer survivors was associated with increased risk for myocardial infarction and cardiomyopathy. Comprehensive dyslipidemia evaluation and treatment are needed to reduce cardiovascular morbidity in this population. [ABSTRACT FROM AUTHOR]

Background. Tenofovir disoproxil fumarate (TDF) or its prodrug, tenofovir alafenamide fumarate (TAF), is currently being recommended in treatment of HIV infection. The distinct pharmacological properties of these two forms of this drug make TAF treatment less nephrotoxic and lead to a better impact on bone density. Nevertheless, a rising concern about TAF's possible metabolic adverse effects exists. This study aimed to evaluate the effects on the lipid profile among ART (antiretroviral therapy) patients switching from a TDF-containing to a TAF-containing regimen in the first year after the switch. Methods. Demographic and clinical data of HIV-positive ART-experienced patients treated in the infectious diseases department was retrospectively collected. Lipid profile change concerning baseline BMI, age, and time of ART duration were analysed. Results. In the group of 36 patients, there was a significant increase in total cholesterol levels (+18.43 mg/dl, SD = 23.86 mg/dl, p < 0.0001) and LDL levels (+13.75 mg/dl, SD = 23.05 mg/dl, p = 0.001) in the first 12 months after switching from a TDF-containing to a TAF-containing regimen. There were no statistically significant changes in both HDL and TG levels observed. Analysis of total cholesterol and LDL levels in specific subpopulations revealed a significant increase within the first year after the switch in patients younger than 40 years old and in those whose BMI was within the normal range. Conclusions. The data suggests that switching from TDF to TAF in ART-experienced patients may be associated with worsening lipid parameters. Early detection and management of dyslipidemias among HIV-positive patients are needed. [ABSTRACT FROM AUTHOR]

Background. Tenofovir disoproxil fumarate (TDF) or its prodrug tenofovir alafenamide fumarate (TAF) are currently being recommended in treatment of HIV infection. Distinct pharmacological properties of these two forms of a this drug make TAF treatment less nephrotoxic and lead to better impact on bone density. Nevertheless, there is a rising concern about possible metabolic adverse effects of TAF. The purpose of this study was to evaluate the effects on the lipid profile among ART (antiretroviral therapy)-experienced patients switching from TDF‑containing to TAF‑containing regimen in the first year after the switch. Methods. Demographic and clinical data of HIV‑positive ART‑experienced patients treated in infectious diseases department was retrospectively collected. Changes of lipid profile with regards to baseline BMI, age and time of ART duration were analyzed. Results. In the group of 36 patients there was a significant increase in total cholesterol levels (+18.43 mg/dl, SD = 23.86 mg/dl, p

Introduction: Androgenic and anabolic action of testosterone mediated through androgen receptor, which have been documented to have significant biological actions in bone, muscle, prostate, adipose tissue and the reproductive, cardiovascular, immune, neural and haemopoietic systems. Aim: Evaluate the action of testosterone on liver histology and lipid profile (cholesterol, triglyceride, LDL, HDL and VLDL). Materials and Methods: Adult female wistar rat (no. 12) and weight (180-200 g) was housed in stain steel cages. Six rats were divided into two groups control group given propylene glycol as vehicle while treated group give testosterone propionate subcutaneous with 100mg/kg dose dissolve in propylene glycol for 30 days. Live histology examination and lipid profile assessment were conducted to compare the differences and the effect of the testosterone. Results: There was no significant differences in all parameters of cholesterol, triglyceride, low-density lipoprotein, high-density lipoprotein and very low-density lipoprotein, while the histology of treated group showed dilatations of the hepatic sinusoids which led to increase pressure of the hepatic biliary system, with fatty changes and dysplasia of hepatocytes. Conclusion: Testosterone plays an important role in aging by increasing hepatic glycogen stores and alteration of hepatic tissues. [ABSTRACT FROM AUTHOR]

Objective Low-density lipoprotein cholesterol (LDL-C) can be estimated using the Friedewald and Martin-Hopkins formulas. We developed LDL-C prediction models using multiple machine learning methods and investigated the validity of the new models along with the former formulas. Methods Laboratory data (n = 59,415) on measured LDL-C, high-density lipoprotein cholesterol, triglycerides (TG), and total cholesterol were partitioned into training and test data sets. Linear regression, gradient-boosted trees, and artificial neural network (ANN) models were formed based on the training data. Paired-group comparisons were performed using a t -test and the Wilcoxon signed-rank test. We considered P values <.001 with an effect size >.2 to be statistically significant. Results For TG ≥177 mg/dL, the Friedewald formula underestimated and the Martin-Hopkins formula overestimated the LDL-C (P  <.001), which was more significant for LDL-C <70 mg/dL. The linear regression, gradient-boosted trees, and ANN models outperformed the aforementioned formulas for TG ≥177 mg/dL and LDL-C <70 mg/dL based on a comparison with a homogeneous assay (P  >.001 vs. P  <.001) and classification accuracy. Conclusion Linear regression, gradient-boosted trees, and ANN models offer more accurate alternatives to the aforementioned formulas, especially for TG 177 to 399 mg/dL and LDL-C <70 mg/dL. [ABSTRACT FROM AUTHOR]

Background: Intracranial aneurysm wall degradation can be associated with lipid infiltration. However, the relationship between lipid infiltration and aneurysm rupture has not been explored quantitatively. To investigate the correlation between lipid infiltration and aneurysm rupture, we utilized patient-specific simulation of low-density lipoprotein (LDL) transport to analyze lipid infiltration in the cerebral aneurysm wall. Methods: Sixty-two aneurysms were analyzed. Patient blood pressure, plasma LDL concentration, and three-dimensional angiographic images were obtained to simulate LDL transport in aneurysms. Morphological, hemodynamic, and lipid accumulation parameters were compared between ruptures and unruptured groups. Multivariate logistic regression was also performed to determine parameters that are independently associated with rupture. Results: Size ratio, wall shear stress, low shear area, relative residence time, area-averaged LDL infiltration rate, and maximum LDL infiltration rate were significant parameters in univariate analysis (P < 0.05). Multivariate analysis revealed that only average LDL infiltration remained as a significant variable (P < 0.05). The prediction model derived showed good performance for rupture prediction (AUC, 0.885; 95% CI, 0.794–0.976). Conclusions: Ruptured aneurysms showed significantly higher LDL infiltration compared to unruptured ones. Our results suggested that lipid infiltration may promote aneurysm rupture. Lipid infiltration characteristics should be considered when assessing aneurysm rupture risk. [ABSTRACT FROM AUTHOR]

This review discusses formation of reactive halogen species (RHS) catalyzed by myeloperoxidase (MPO), an enzyme mostly present in leukocytes. An imbalance between the RHS production and body's ability to remove or neutralize them leads to the development of halogenative stress. RHS reactions with proteins, lipids, carbohydrates, and antioxi-dants in the content of low-density lipoproteins (LDLs) of the human blood are described. MPO binds site-specifically to the LDL surface and modifies LDL properties and structural organization, which leads to the LDL conversion into proatherogenic forms captured by monocytes/macrophages, which causes accumulation of cholesterol and its esters in these cells and their transformation into foam cells, the basis of atherosclerotic plaques. The review describes the biomarkers of MPO enzymatic activity and halogenative stress, as well as the involvement of the latter in the development of atherosclerosis. [ABSTRACT FROM AUTHOR]

Background: Primary aldosteronism (PA) may confer increased cardiovascular risk beyond effects on systemic blood pressure, but contributing mechanisms remain incompletely understood. We compared plasma (apo)lipoproteins and lipoprotein particle characteristics, GlycA, a pro‐inflammatory glycoprotein biomarker of enhanced chronic inflammation, and plasma total branched‐chain amino acids (BCAA), measured using nuclear magnetic resonance (NMR) spectroscopy, between patients with PA, control subjects without hypertension, subjects with untreated hypertension and subjects with treated hypertension. Methods: Twenty PA patients were individually matched with 2819 control subjects without hypertension, 501 subjects with untreated hypertension and 878 subjects with treated hypertension participating in the PREVEND (Prevention of Renal and Vascular End‐Stage Disease) cohort study with respect to age, sex, body mass index, smoking and statin use. The Vantera® Clinical Analyzer was used to determine NMR‐based laboratory parameters. Results: Total cholesterol, low‐density lipoprotein cholesterol (LDL‐C), high‐density lipoprotein cholesterol (HDL‐C), apolipoprotein (apo) B, apolipoprotein A‐I (apoA‐I), LDL particle and HDL particle concentrations were all decreased in PA subjects vs control subjects and subjects with untreated hypertension (P < 0.016). Triglycerides (TG) and triglyceride‐rich lipoprotein (TRL) concentrations were lower in PA subjects vs subjects with (untreated) hypertension. GlycA was increased in PA vs the three comparator groups (P < 0.016). Total BCAA concentrations were unaltered in PA. Conclusions: Primary aldosteronism is associated with lower concentrations of LDL and HDL particles and to some extent also with lower TG and TRL particle concentrations. PA is also characterized by increased GlycA levels, indicating enhanced low‐grade chronic inflammation. Low HDL particle concentrations and increased GlycA could contribute to accelerated cardiovascular disease development in PA. [ABSTRACT FROM AUTHOR]

People who maintain ideal cardiovascular heath have a low lifetime risk of cardiovascular disease. Therefore, encouraging people to achieve ideal cardiovascular health represents an important opportunity to improve the prevention of cardiovascular disease. However, preventing cardiovascular disease by promoting ideal cardiovascular health requires shifting the focus from treating disease after it develops to preventing cardiovascular events before they happen by slowing the progression of atherosclerosis. Because atherogenic lipoproteins play a central causal role in the initiation and progression of atherosclerosis, maintaining optimal lipid levels is necessary to achieve ideal cardiovascular health. This review describes the cumulative effect of lipid-carrying lipoproteins on the risk of cardiovascular disease, estimates the magnitude of the clinical benefit that can be achieved by maintaining optimal lipid levels, identifies the most effective timing for implementing strategies designed to achieve optimal lipid levels, and provides a clinical pathway to help people achieve the lipid levels necessary for ideal cardiovascular health. [ABSTRACT FROM AUTHOR]

Summary: Aim: PCSK9 inhibitors (PCSK9i) effectively lower cholesterol levels in randomized trials with reduction in cardiovascular outcomes and favorable safety profile. However, the access to PCSK9i is limited due to high cost and data regarding the use of PCSK9i in real‐world practice is limited. Methods: Data on all patients submitted for approval of PCSK9i at a regional lipid clinic, outside of clinical trials. Patients' profile, approval rates, low‐density lipoprotein cholesterol (LDL‐C) reduction rates, and adverse events were evaluated. Results: Recommendation for PCSK9i was given to 133 patients; 16 did not receive insurance approval and additional 16 were approved but did not initiate therapy. Of the 101 treated patients (47% females; mean age 61 ± 11 years), 52 had probable/definite familial hypercholesterolemia (FH) (peak LDL‐C level 305 ± 87 mg/dL vs non‐FH 204 ± 39 mg/dL) and 62% had an established cardiovascular disease. Statin intolerance was reported by 77%. Follow‐up lipid panel was available in 66/101 patients: mean LDL‐C reduction was 59% ± 19. Subjects with heterozygous FH had similar LDL‐C decrease than those with non‐FH (59% ± 22 vs 60% ± 14, P = .792). LDL‐C < 100 mg/dL was achieved by 76%, LDL‐C < 70 mg/dL by 58% and LDL‐C < 40 mg/dL by 18% of those with follow‐up data. Side effects were reported by 10%, mainly musculoskeletal complaints and flu‐like symptoms, and 15% have discontinued treatment. Conclusions: Patient selection by a regional lipid clinic resulted in a high real‐world PCSK9i insurance approval, with efficacy and safety comparable to randomized clinical trials. Cost and medication nonadherence are potential barriers to successful implementation of therapy in routine clinical care. [ABSTRACT FROM AUTHOR]

Purpose Of Review: This article reviews current knowledge concerning diabetic dyslipidemia and cardiovascular disease (CVD). It reviews strategies to reduce diabetes-associated CVD, including reducing low-density lipoprotein levels, lowering triglycerides, and increasing high-density lipoproteins (HDL). Special considerations, such as the multifactorial chylomicronemia syndrome and partial lipodystrophy, and the role of glucose-lowering strategies in the management of diabetic dyslipidemia are discussed.Recent Findings: The strongest evidence to date for reducing CVD in diabetes comes from the use of statins. While triglyceride lowering remains inconclusive, an ongoing trial might provide some finality to this question. The role of increasing HDL remains elusive, and HDL cholesterol appears to be an unsatisfactory metric for monitoring therapy. The use of statins offers the best current way to reduce diabetes-associated CVD. However, several novel and promising approaches for the management of diabetic dyslipidemia aimed at reducing CVD are in the pipeline. [ABSTRACT FROM AUTHOR]

Incidence of diabetes with its associated morbidities is increasing worldwide and hence needs major lifestyle modifications. Hence, this study was designed to compare the effect of moderate intensity exercise for a shorter period of time with an active lifestyle to a low-intensity exercise for a longer period of time and sedentary lifestyle on the lipid profile of diabetic men. The outpatients of MV Hospital were screened using a structured questionnaire to evaluate their lifestyle and exercise pattern over a period of 12 months. The data of 293 men and women were divided into three groups based on their activity level. Group 1 led a totally sedentary lifestyle with no exercise. Group 2 included individuals who were active throughout the day and walked at moderate intensity for a period of 20-30 min, and group 3 exercised at a low intensity for a period of 45-60 min with a sedentary lifestyle. The anthropometric measurements and the lipid profiles of the three groups were compared. A total 41.8 % of the group which led an active lifestyle as well as a moderate intensity of exercise had good glycemic control. The non-HDL levels were 131 ± 38.4 which was significantly lower than the other groups. Hence, the group which led an active lifestyle with moderate intensity exercise fared better than the sedentary group. An active lifestyle throughout the day with an exercise schedule of moderate intensity maintains the lipid parameters more effectively than a low-intensity exercise for a much longer period of time. [ABSTRACT FROM AUTHOR]

Earlier reports indicated that patients with the apolipoprotein APOE ε4 allele responded to fish oil supplementation with a rise in serum low-density lipoprotein cholesterol (LDL-C) compared to ε3 homozygotes. In this study, we used clinical laboratory data to test the hypothesis that the cross-sectional relation between RBC omega-3 fatty acid status (the Omega-3 Index) and LDL-C was modified by APOE genotype. Data from 136,701 patients were available to compare lipid biomarker levels across Omega-3 Index categories associated with heart disease risk in all APOE genotypes. We found no adverse interactions between APOE genotype and the Omega-3 Index for LDL-C, LDL particle number, apoB, HDL-C, or triglycerides. However, we did find evidence that ε2 homozygotes lack an association between omega-3 status and LDL-C, apoB, and LDL particle number. In summary, we found no evidence for a deleterious relationship between lipid biomarkers and the Omega-3 Index by APOE genotype. [ABSTRACT FROM AUTHOR]

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In this work we introduce and discuss several mathematical models, based on partial differential equations, devised to study the coupled transport of macromolecules as low-density lipoproteins in the blood stream and in the arterial walls. These models are accurate provided that a suitable set of physical parameters characterizing the physical properties of the molecules and of the wall layers are available. Here we turn our attention on this aspect, and propose a new methodology to compute the physical parameters needed for the model set up, starting from available in vivo measurements. Then, we focus on the study of the accumulation of low-density lipoproteins in vascular districts featuring a highly disturbed flow.Our results demonstrate that mathematical models whose set up procedure benefits from an experimental feedback provide reliable information not only qualitatively, but also quantitatively. Their application to geometrically perturbed vascular districts (as for example a severe stenosis) shows that geometrical parameters such as curvature and variations of the lumenal section strongly influence the accumulation of low-density lipoproteins within the wall. For instance, in a stenotic segment with 75% area constriction, the LDL concentration at the lumenal side of the wall is about 10% higher than for the undisturbed segment. [Copyright &y& Elsevier]

Aims/hypothesis: Previous studies have implicated the glycoxidative modification of low-density lipoprotein (LDL) by glucose and aldehydes (apparently comprising both glycation and oxidation), as a causative factor in the elevated levels of atherosclerosis observed in diabetic patients. Such LDL modification can result in unregulated cellular accumulation of lipids. In previous studies we have characterized the formation of glycated, but nonoxidized, LDL by glucose and aldehydes; in this study we examine whether glycation of LDL, in the absence of oxidation, gives rise to lipid accumulation in arterial wall cell types. Methods: Glycated LDLs were incubated with macrophage, smooth muscle, or endothelial cells. Lipid loading was assessed by HPLC analysis of cholesterol and individual esters. Oxidation was assessed by cholesterol ester loss and 7-ketocholesterol formation. Cell viability was assessed by lactate dehydrogenase release and cell protein levels. Results: Glycation of LDL by glycolaldehyde and methylglyoxal, but not glucose (in either the presence or absence of copper ions), resulted in cholesterol and cholesterol ester accumulation in macrophage cells, but not smooth muscle or endothelial cells. The extent of lipid accumulation depends on the degree of glycation, with increasing aldehyde concentration or incubation time, giving rise to greater extents of particle modification and lipid accumulation. Modification of lysine residues appears to be a key determinant of cellular uptake. Conclusions/interpretation: These results are consistent with LDL glycation, in the absence of oxidation, being sufficient for rapid lipid accumulation by macrophage cells. Aldehyde-mediated "carbonyl-stress" may therefore facilitate the formation of lipid-laden (foam) cells in the artery wall. [ABSTRACT FROM AUTHOR]

Ethanol has a pronounced effect on lipid homeostasis. It is our overall hypothesis that certain lipid carrier proteins are targets of acute and chronic ethanol exposure and that perturbation of these proteins induces lipid dysfunction leading to cellular pathophysiology. These proteins include both intracellular proteins and lipoproteins. This paper examines recent data on the interaction of ethanol with these proteins. In addition, new data are presented on the stimulatory effects of ethanol on low-density-lipoprotein (LDL)-mediated cholesterol uptake into fibroblasts and direct perturbation of the LDL apolipoprotein, apolipoprotein B. A cell model is presented that outlines potential mechanisms thought to be involved in ethanol perturbation of cholesterol transport and distribution.Copyright © 2001 National Science Council, ROC and S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which explores the association between paraoxonase 2 sequence variation and the decrease in circulating low-density lipoprotein (LDL) size in children and adolescents.

Lipid markers are well-established predictors of vascular disease. The most frequently measured lipid markers are total cholesterol, high-density lipoprotein (HDL)-cholesterol (HDL-C), LDL cholesterol (LDL-C), and triglyceride. HDL reduces atherosclerosis by multiple mechanisms, leading to a reduced risk of cardiovascular disease, and HDL-C, as a metric of HDL quantity, is inversely associated with cardiovascular disease, independent of LDL-C. However, the quality of the HDL appears to be more important than its quantity, because HDL loses its antiatherogenic functions due to changes in its composition and becomes "dysfunctional HDL". Although there is evidence of the existence of "dysfunctional HDL", biomarkers for monitoring dysfunctional HDL in clinical practice have not yet been established. In this review, we propose a new lipid panel for the assessment of dysfunctional HDL and lipoprotein-related atherosclerotic cardiovascular disease. The lipid panel includes the measurement of lipid peroxide and triglyceride contents within HDL particles. [ABSTRACT FROM AUTHOR]

Background Integrase strand transfer inhibitor (INSTI)-based antiretroviral therapy (ART) is recommended first-line HIV treatment. We recently demonstrated increased weight gain associated with INSTI use among women living with HIV (WLH) enrolled in the Women's Interagency HIV Study (WIHS), raising concern for cardiometabolic consequences. We, therefore, evaluated the effects of INSTI use on lipids, insulin resistance, and glycemic control in WLH. Methods Data from 2008 to 2017 were analyzed from WLH enrolled in WIHS. Women who switched to or added an INSTI to ART (SWAD group) were compared with women who remained on non-INSTI ART (STAY group). Outcomes included changes in fasting total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides (TG), and glucose; hemoglobin A1c; and incident insulin resistance (defined as homeostatic model assessment of insulin resistance [HOMA] score ≥2). Outcomes were measured 6–12 months before and 6–18 months after INSTI switch/add in the SWAD group with comparable time points in the STAY group. Linear regression models compared change over time in each outcome by SWAD/STAY group, adjusted for age, race, WIHS site, income, smoking status, statin use, and ART regimen at baseline. Results In total, 881 WIHS participants (182 SWAD and 699 STAY) were followed for a mean 1.8 (±1.1) years. Mean age was 49 (±8.8) years, BMI was 31 (±8.2) kg/m2, and 49% were Black. At baseline, SWAD vs. STAY was more likely to report NNRTI (vs. PI)-based ART and statin use (both P < 0.0001), but all baseline lipid and glucose variables were similar. Compared with STAY, the SWAD group experienced significantly greater decreases in HDL (−2.4 vs. +0.09 mg/dL, P = 0.03) and trended toward greater decreases in TC (−2.6 vs. −2.4 mg/dL, P = 0.07) at follow-up, without significant differences in TG or LDL. The SWAD group had significantly greater increases in A1c (+0.08% vs. −0.05%, P = 0.01) but trended toward lower incidence of insulin resistance (19% vs. 32%, P = 0.05). Conclusion Despite reported increases in weight, INSTI use was associated with only modest changes in lipid measurements and glycemic control during short-term follow-up of WLH compared with non-INSTI ART. Research is needed to elucidate long-term cardiometabolic effects. Disclosures Anandi N. Sheth, MD, MS, Gilead Sciences, Inc.: Research Grant. [ABSTRACT FROM AUTHOR]

Background Vitamin D deficiency is associated with an unfavorable lipid profile, but whether and how vitamin D supplementation affects lipid metabolism is unclear. Objective To examine the effects of vitamin D supplementation on lipid and lipoprotein parameters. Methods This is a post hoc analysis of the single-center, double-blind, randomized, placebo-controlled Styrian Vitamin D Hypertension Trial (2011–2014). Two hundred individuals with arterial hypertension and 25-hydroxyvitamin D concentrations of <75 nmol/L were randomized to 2800 IU of vitamin D daily or placebo for 8 weeks. Results One hundred sixty-three participants (62.2 [53.1–68.4] years of age; 46% women) had available lipid data and were included in this analysis. Vitamin D supplementation significantly increased total cholesterol, triglycerides, very-low-density lipoprotein (VLDL) triglycerides, low-density lipoprotein (LDL) triglycerides, high-density lipoprotein (HDL) triglycerides, apolipoprotein B (ApoB), LDL-ApoB, ApoCII, ApoCIII, phospholipids, and ApoE ( P < .05 for all). Except for ApoCII and ApoCIII and HDL-triglycerides, all other treatment effects remained statistically significant after adjustment for multiple testing with the Benjamini and Hochberg false discovery rate method. There was a nonsignificant increase in LDL cholesterol. Furthermore, no significant effects were seen on free fatty acids, lipoprotein (a), ApoAI, ApoAII, VLDL cholesterol, VLDL–ApoB, HDL cholesterol, LDL diameter, and VLDL diameter. Conclusions The effects of vitamin D on lipid metabolism are potentially unfavorable. They require further investigation in view of the wide use of vitamin D testing and treatment. [ABSTRACT FROM AUTHOR]