Low-density Lipoprotein Size Research Articles

Smaller low‐density lipoprotein size as a possible risk factor for the prevalence of coronary artery diseases in haemodialysis patients: Associations of cholesteryl ester transfer protein and the hepatic lipase gene polymorphism with low‐density lipoprotein size

Smaller low-density lipoprotein (LDL) size has recently been reported as a non-traditional lipid risk factor for coronary artery disease (CAD). Cholesteryl ester transfer protein (CETP) and the C/T hepatic lipase (HL) gene polymorphism may promote LDL size reduction via the CETP-mediated exchange of CE for triglyceride (TG) and subsequent HL-mediated TG hydrolysis in LDL. However, little is known about LDL size status and its relationship with CAD prevalence in haemodialysis (HD) patients who are at high risk for atherosclerosis. CETP levels, HL genotypes and LDL size were determined, and the determinants of LDL size and its association with CAD prevalence in HD patients (n = 236) aged over 30 years were investigated. The HD patients had a similar LDL size to the healthy subjects. In the HD group, high-density lipoprotein cholesterol was an independent positive determinant of LDL size, while log(10) (TG) was an independent negative determinant in the high (≥2.1 µg/mL) but not low (<2.1 µg/mL) CETP group. In the patients with hypertriglyceridemia, the high CETP group had a significantly smaller LDL size than the low CETP group. Among the patients with above-median TG levels, the CC genotype and CETP were independent negative determinants of LDL size. In the whole group and the high CETP group, the patients with CAD had a significantly smaller LDL size than those without CAD. Finally, DM and smaller LDL size were identified as independent risk factors for CAD prevalence. These suggest that a smaller LDL size, which is associated with higher levels of TG and CETP and the HL/CC genotype, may serve as a risk factor for CAD in HD patients.

Effect of three consecutive meals on the physicochemical properties of HDL and LDL in individuals with the metabolic syndrome and patients with type 2 diabetes

Postprandial hyperlipidemia, which is exaggerated and prolonged in insulin-resistant individuals, has been associated with cardiovascular disease. The objective of this study was to investigate whether and how the composition, size and function of high-density lipoprotein (HDL) and low-density lipoprotein (LDL) particles are affected in the postprandial state among males with the metabolic syndrome (MetS) or type 2 diabetes (T2DM), compared with controls. A total of 14 males with T2DM, 14 with the MetS and 14 age-matched controls were given three standardized high-fat mixed meals (900 kcal; 50-g fat, 75-g carbohydrate and 35-g protein) as breakfast, lunch and dinner. Blood sampling was performed just before each meal, and 4 and 8 h after the last meal. HDL and LDL were isolated by ultracentrifugation and analyzed for their composition, particle diameter and functional properties. Postprandial triglycerides levels in plasma, HDL and LDL particles increased significantly in all groups (P<0.01). Compared with the control subjects, patients with T2DM had smaller LDL particles, and in agreement, a lower cholesterol-to-protein content in both fasting and postprandial samples. A prolonged increase in susceptibility of LDL to oxidation was found in all subjects, but was most evident in T2DM. The postprandial effect on LDL oxidation was associated with an increase in LDL triglyceride (r=0.29, P<0.05). In T2DM the anti-oxidative capacity of HDL trended to impairment after the third meal. Postprandial increases in triglycerides, especially in T2DM, are accompanied by pro-atherosclerotic functional changes in HDL and LDL particles.

Polycystic ovary syndrome is associated with atherogenic changes in lipoprotein particle number and size independent of body weight

Adverse changes in lipoprotein particle number and size are common with insulin resistance and are associated with increased cardiovascular risk. Comprehensive information regarding lipoprotein particle number and size, and how these parameters relate to body weight, insulin resistance and hyperandrogenemia is lacking in polycystic ovary syndrome (PCOS). We tested the hypothesis that PCOS is associated with atherogenic changes in lipoprotein profile independent of body weight and examined the role of insulin resistance and androgens in these atherogenic changes. Case-control study performed at Clinical Research Center at an Academic Medical Center in the United States. Fasting blood was obtained from 25 PCOS and 25 control women of similar age and body mass index (BMI). Lipoprotein particle number and size was determined by nuclear magnetic resonance and compared between the groups. The mean BMI for both groups was <30 kg/m(2) (P = 0·33). Women with PCOS had an increase in very low-density lipoprotein (VLDL) particle number (P = 0·005), low-density lipoprotein (LDL) particle number (P = 0·02) and a decrease in high-density lipoprotein (HDL) size (P = 0·04). LDL size was borderline decreased (P = 0·09). These differences persisted after adjustment for ethnicity, alcohol and tobacco intake and exercise. In stepwise regression models, bioavailable testosterone was the only predictor of LDL cholesterol, triglyceride, VLDL and LDL particle number. Sex hormone binding globulin (SHBG) was the only predictor of LDL and HDL size. Independent of body weight, PCOS was associated with changes in lipoprotein profile that increases risk for cardiovascular disease. These changes were present in a mostly nonobese group of women and were more closely related to androgens than fasting insulin.

Abnormal High-Density Lipoproteins in Overweight Adolescents With Atherogenic Dyslipidemia

This study aimed to evaluate high-density lipoprotein functionality and the cardiovascular risk factor profile in the overweight pediatric population. We hypothesized that overweight adolescents with low high-density lipoprotein cholesterol and elevated triglyceride plasma levels have metabolic abnormalities and dysfunctional high-density lipoprotein particles, similar to those reported in adults. Overweight adolescents with (group 1 [n = 21]) and without (group 2 [n = 36]) atherogenic dyslipidemia (high-density lipoprotein cholesterol: ≤ 40 mg/dL and triglycerides: ≥ 150 mg/dL) and normal-weight normolipidemic subjects, as a reference (group 3 [n = 36]), were included. The cardiovascular risk factor profile (lipids, lipoproteins, high-sensitivity C-reactive protein, and insulin), high-density lipoprotein subclass distribution, composition, and cholesterol efflux capacity were studied. Group 1 adolescents showed abnormalities in high-density lipoprotein subclass distribution and high-density lipoprotein chemical composition, as well as a significantly lower capacity to promote cholesterol efflux (14.8 ± 2.8, 16.5 ± 3.8, 20.4 ± 3.5, for groups 1, 2 and 3, respectively). High-density lipoprotein(2a) (R(2) = 0.212, β = 0.472, P < .0001) and the Tanner score (R(2) = 0.054, β = -0.253, P = .02) were the independent predictors of cholesterol efflux. Group 1 also showed a higher degree of cardiovascular abnormalities (an adverse lipoprotein profile, greater insulin resistance and systemic inflammation; and lower low-density lipoprotein size) than group 2, even after BMI and Tanner score adjustment. This study suggests that atherogenic dyslipidemia identifies overweight adolescents with quantitative, qualitative, and functional high-density lipoprotein abnormalities. Atherogenic dyslipidemia seems to be a marker of an increased risk for developing cardiovascular disease and indicates that those adolescents should be a target of aggressive prevention programs and lipid management guidelines.

Atherogenic Lipid Profile in Behçet’s Disease: Evidence of Alteration of HDL Subclasses

Behçet's disease (BD) is an inflammatory vasculitis, most common in the Mediterranean area and Asia. Evidence for accelerated atherosclerosis in BD has been observed. The relationship between cardiovascular risk factors and accelerated atherosclerosis in patients with BD is still controversial. The aim of this study was to evaluate the lipid profile and to investigate the low-density lipoprotein (LDL) size and the distribution of high-density lipoprotein (HDL) subpopulations in BD patients. Thirty six BD patients were compared to 36 healthy controls. Total cholesterol (TC), triglycerides (TG) and HDL-cholesterol (HDL-C) levels were measured using standard techniques. HDL subclasses and LDL-C size were estimated using polyacrylamide linear gradient gel electrophoresis. The LDL-C/HDL-C ratio was also calculated. High-sensitive C-reactive protein (hsCRP) level was measured by a turbidimetric method. Homocysteine (Hcy) level was determined using a liquid chromatography tandem mass spectrometry (LC/MS/MS). In BD patients, HDL-C levels as well as its subfraction levels were decreased (respectively, p <10(-6) and p <10(-3)). Percentage of HDL2 subpopulation was also decreased (p=0.02). HDL3 subfraction was significantly higher (p=0.02). The LDL-C/HDL-C ratio and CRP level were increased (respectively, p=10(-4) and p=0.003). TC was correlated with CRP. HDL-C and its subfractions were correlated with CRP and TG levels. HDL subparticle percentages were also correlated with age. Our findings of a reduction of HDL-C and HDL2 subpopulation and an increase HDL3 subclass and a higher LDL-C/HDL-C ratio may be considered as important predictors of cardiovascular events in BD patients.

Observational study of lipid profile and LDL particle size in patients with metabolic syndrome

BackgroundThe atherogenic lipoprotein phenotype is characterized by an increase in plasma triglycerides, a decrease in high-density lipoprotein cholesterol (HDLc), and the prevalence of small, dense-low density lipoprotein cholesterol (LDLc) particles. The aim of this study was to establish the importance of LDL particle size measurement by gender in a group of patients with Metabolic Syndrome (MS) attending at a Cardiovascular Risk Unit in Primary Care and their classification into phenotypes.Subjects and methodsOne hundred eighty-five patients (93 men and 92 women) from several areas in the South of Spain, for a period of one year in a health centre were studied. Laboratory parameters included plasma lipids, lipoproteins, low-density lipoprotein size and several atherogenic rates were determinated.ResultsWe found differences by gender between anthropometric parameters, blood pressure and glucose measures by MS status. Lipid profile was different in our two study groups, and gender differences in these parameters within each group were also remarkable, in HDLc and Apo A-I values. According to LDL particle size, we found males had smaller size than females, and patients with MS had also smaller than those without MS. We observed inverse relationship between LDL particle size and triglycerides in patients with and without MS, and the same relationship between all atherogenic rates in non-MS patients. When we considered our population in two classes of phenotypes, lipid profile was worse in phenotype B.ConclusionIn conclusion, we consider worthy the measurement of LDL particle size due to its relationship with lipid profile and cardiovascular risk.

Effects of smoking and smoking cessation on lipids and lipoproteins: Outcomes from a randomized clinical trial

the effects of smoking and smoking cessation on lipoproteins have not been studied in a large contemporary group of smokers. This study was designed to determine the effects of smoking cessation on lipoproteins. this was a 1-year, prospective, double-blind, randomized, placebo-controlled clinical trial of the effects of 5 smoking cessation pharmacotherapies. Fasting nuclear magnetic resonance spectroscopy lipoprotein profiles were obtained before and 1 year after the target smoking cessation date. The effects of smoking cessation and predictors of changes in lipoproteins after 1 year were identified by multivariable regression. the 1,504 current smokers were (mean [SD]) 45.4 (11.3) years old and smoked 21.4 (8.9) cigarettes per day at baseline. Of the 923 adult smokers who returned at 1 year, 334 (36.2%) had quit smoking. Despite gaining more weight (4.6 kg [5.7] vs 0.7 kg [5.1], P < .001], abstainers had increases in high-density lipoprotein cholesterol (HDL-C) (2.4 [8.3] vs 0.1 [8.8] mg/dL, P < .001), total HDL (1.0 [4.6] vs -0.3 micromol/L [5.0], P < .001), and large HDL (0.6 [2.2] vs 0.1 [2.1] micromol/L, P = .003) particles compared with continuing smokers. Significant changes in low-density lipoprotein (LDL) cholesterol and particles were not observed. After adjustment, abstinence from smoking (P < .001) was independently associated with increases in HDL-C and total HDL particles. These effects were stronger in women. despite weight gain, smoking cessation improved HDL-C, total HDL, and large HDL particles, especially in women. Smoking cessation did not affect LDL or LDL size. Increases in HDL may mediate part of the reduced cardiovascular disease risk observed after smoking cessation.

Carbohydrate‐ vs Fat‐Controlled Diet Effect on Weight Loss and Coronary Artery Disease Risk

This pilot study compared weight loss and serum indicators of coronary artery disease (CAD) risk between 2 weight loss (energy-deficit) diets, one controlled for carbohydrate as a percentage of total calories and the other controlled for fat as percentage of total calories. Participants were randomized to 1 of 2 diets and fed on an outpatient basis for 70 days, after which they followed their diets using their own resources for an additional 70 days. Energy deficit for the diets was determined by indirect calorimetry with a 500- to 750-calorie per day adjustment. Weight and CAD risk indicators and serum lipid and C-reactive protein levels were measured at baseline, day 70, and day 140. The study was completed by 16 of 20 participants who were able to comply with the feeding portion of the study as well as with follow-up appointments during the second (self-management) period of the study. Participants lost weight in both diet groups (24.4 lbs, carbohydrate controlled; 18.5 lbs, fat controlled), and serum CAD risk factors decreased in both groups. There were no significant differences in CAD risk factors between diet groups, although there was a trend toward lighter low-density lipoprotein (LDL) size in the carbohydrate-controlled group. During the self-management portion of the study, weight loss stalled or regained from loss during the previous feeding period. The results, although underpowered, are consistent with recent studies in which macronutrient ratio of total calories in diet did not affect degree of weight loss and in which carbohydrate-controlled diets produced a predominance of lighter LDLs.

Effects of atorvastatin versus probucol on low-density lipoprotein subtype distribution and renal function in hyperlipidemic patients with nondiabetic nephropathy

Objectives: Small dense low-density lipoprotein (LDL) plays an important role in glomerular injury through conversion to an oxidatively modified form of LDL. However, few studies have evaluated the effects of antilipidemic agents on the LDL particle size and renal function in hyperlipidemic patients with nondiabetic nephropathy. Methods: This study was a randomized crossover trial comparing the effects of atorvastatin (10 mg/day) and probucol (500 mg/day) administered for 24 weeks in 31 patients (urinary albumin excretion 0.3–2.0 g/day and creatinine clearance >30 mL/min/1.73 m). Lipid parameters, mean LDL particle diameter, creatinine clearance, and urinary albumin to creatinine excretion ratio were measured before and during treatment periods. Main findings: Atorvastatin and probucol significantly reduced the serum total cholesterol and LDL cholesterol concentrations. When stratified by mean baseline LDL particle size at 25.5 nm, atorvastatin increased (p < 0.05) LDL particle size from 24.6 ± 0.5 to 25.2 ± 0.9 nm only in the <25.5 nm (pattern B) group, whereas probucol decreased (p < 0.05) LDL size from 24.8 ± 0.9 to 24.2 ± 0.9 nm in the pattern B group and from 25.9 ± 0.5 to 24.6 ± 0.8 nm in the ≥25.5 nm (pattern A) group. No significant differences in urinary albumin/creatinine excretion ratio and creatinine clearance were observed in both groups during treatment. Conclusions: Only atorvastatin improved the LDL-subtype distribution in hyperlipidemic patients with nondiabetic nephropathy, although both agents exhibited no renoprotective action, suggesting that the effects on LDL-subtype distribution do not directly lead to renoprotection.

Effects of Rosiglitazone on Fasting and Postprandial Low- and High-Density Lipoproteins Size and Subclasses in Type 2 Diabetes

Rosiglitazone may increase cardiovascular risk in patients with type 2 diabetes. Yet, its effects on atherogenic dyslipidemia are still not fully elucidated. In a prospective open-label study rosiglitazone (4 mg/day for 12 weeks) was added to a maximum of 2 oral antidiabetic drugs in 18 diabetic patients. We evaluated the effects on plasma lipids before and after an oral fat load. The size and subclasses of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) were also determined (by gradient gel electrophoresis). Rosiglitazone improved glycosylated hemoglobin ([HbA1c] P = .0023), without significant effects on fasting and postprandial plasma lipids. Fasting LDL size increased (+1.4%, P = .034), with less small, dense LDL-IIIA (-25.1%, P = .018). Postprandially, larger HDL-2b reduced (-8.7%, P = .006) and smaller HDL-3b increased (+12.2%, P = .05), without any effects on HDL size. Rosiglitazone led to antiatherogenic changes in LDL size and subclasses, with proatherogenic changes in HDL subclasses, despite no effects on plasma lipids. Their clinical relevance remains to be established.

Low-Density Lipoprotein Size and Lipoprotein-Associated Phospholipase A2 in HIV-Infected Patients Switching to Abacavir or Tenofovir

The aim of this study was to assess changes in the size and cholesterol content of low-density lipoproteins (LDL) and changes in lipoprotein-associated phospholipase A2 (Lp-PLA2) activity in HIV-infected patients switching to tenofovir + emtricitabine (TDF+FTC) or abacavir + lamivudine (ABC+3TC). This was a substudy of a multicentre randomized trial comparing TDF+FTC with ABC+3TC-based regimens in patients with virological suppression. Fasting lipids and apolipoproteins (apo), LDL size and cholesterol content and Lp-PLA2 activity were measured at baseline and at week 48. A total of 62 patients, naive for the compared drugs, were included. At baseline, groups were comparable except for total Lp-PLA2 activity (P=0.047) and for a tendency towards the use of a major baseline thymidine analogue in the TDF+FTC arm (25 versus 18 patients; P=0.054). In the ABC+3TC arm a significant increase in total cholesterol (0.64 mmol/l; P=0.003), high-density lipoprotein cholesterol (HDL-c, 0.13 mmol/l; P=0.031), triglycerides (0.39 mmol/l; P=0.036), apo A-I (0.12 g/l; P=0.006), apo B (0.16 g/l; P=0.015) and non-HDL-c (0.50 mmol/l; P=0.009) concentrations was observed at week 48 compared with the TDF+FTC treatment arm. In addition, an increase in the cholesterol content of small, dense LDL subfractions (0.48 mmol/l; P=0.003) and a decrease in LDL size (-2.6 nm; P=0.011) was observed in the ABC arm without changes in the TDF patients. Total PLA2, LDL-PLA2 and HDL-PLA2 activity decreased in the TDF arm, but multivariate analysis showed baseline PLA2 values and previous use of thymidine analogues as the factors associated with these changes. Estimated cardiovascular risk did not change in either arm. A more atherogenic LDL profile, including a decrease in LDL size, was found in the ABC group and not in TDF patients.

FABP4 plasma levels are increased in familial combined hyperlipidemia

FABP4 plasma levels are increased in familial combined hyperlipidemia

Elevated depressive symptoms and compositional changes in LDL particles in middle-aged men

Depression and cardiovascular disease (CVD) are closely associated, but the mechanisms underlying this connection are unclear. Regardless of the low cholesterol levels observed in depression, a small particle size of low-density lipoproteins (LDL), as well as elevated apolipoprotein B (ApoB) levels, are related to increased CVD risk, even when levels of LDL cholesterol are low. We examined the association between elevated depressive symptoms and compositional changes in serum LDL particles in a sample of 2,456 middle-aged Finnish men. Depressive symptoms were assessed with the 18-item Human Population Laboratory Depression Scale, and the study population was divided into two groups (elevated depressive symptoms, n = 269; non-depressed, n = 2,187). The levels of serum total cholesterol (TC), low- and high-density lipoprotein cholesterol (LDL-C, HDL-C), triglycerides (TG), and ApoB were determined. The LDL-C/ApoB ratio, a marker of compositional changes in LDL particle size, was calculated. The group with elevated depressive symptoms had lowered levels of serum TC (P = 0.028) and LDL-C (P = 0.008). No differences were observed in the LDL-C/ApoB ratio. The likelihood for belonging to the group with elevated depressive symptoms increased 10% for each 0.5 mmol/l decrease in the levels of TC (P = 0.002) or LDL-C (P = 0.001) in regression models adjusted for age, examination years, marital and socioeconomic status, energy expenditure, body mass index, CVD history, alcohol consumption, smoking, and the use of lipid-lowering, antidepressant and antipsychotic medications. Our findings suggest that greater small-particle LDL levels are not associated with depression, and are thus unlikely to underlie the association between cardiovascular risk and depression.

FABP4 plasma levels are increased in familial combined hyperlipidemia

The lipid profile of familial combined hyperlipidemia (FCHL) shares some characteristics with atherogenic dyslipidemia seen in diabetes, metabolic syndrome, and obesity. Adipocyte fatty acid-binding protein 4 (FABP4) appears to be a determinant of atherogenic dyslipidemia. We examined relationships between FABP4 plasma concentrations, dyslipidemia, and metabolic variables in patients with FCHL. We studied 273 unrelated FCHL patients and 118 control subjects. FABP4 was higher in FCHL than controls, with mean levels of 21.8 (10.1) microg/l and 19.2 (9.2) microg/l, respectively (adjusted P= 0.012). In FCHL, FABP4 correlated to body mass index (BMI), waist circumference, insulin levels, and homeostasis model assessment (HOMA) index (all P< 0.05), but not to lipid levels, whereas in obese patients, FABP4 correlated to triglyceride levels (r = 0.303, P= 0.014) and very low density lipoprotein size (r = 0.502, P = 0.001), as determined by nuclear magnetic resonance. Associations of FABP4 with BMI and waist circumference, but not with insulin levels, persisted in this subgroup. Plasma FABP4 does not influence the lipid phenotype of FCHL. In a small subgroup of obese FCHL, FABP4 levels were associated with triglyceride-rich lipoproteins independent of insulin resistance. These results support a hyperlipidemic mechanism of FCHL different from similar metabolic conditions where fat mass is strongly related to FABP4 and hypertriglyceridemia.

Linkage and association analyses identify a candidate region for apoB level on chromosome 4q32.3 in FCHL families

Familial combined hyperlipidemia (FCHL) is a complex trait leading to cardiovascular disease (CVD) risk. Elevated levels and size of apolipoprotein B (apoB) and low-density lipoprotein (LDL) are associated with FCHL, which is genetically heterogeneous and is likely caused by rare variants. We carried out a linkage-based genome scan of four large FCHL pedigrees for apoB level that is independent of LDL: apoB level that is adjusted for LDL level and size. Follow-up included SNP genotyping in the region with the strongest evidence of linkage. Several regions with the evidence of linkage in individual pedigrees support the rare variant model. Evidence of linkage was strongest on chromosome 4q, with multipoint analysis in one pedigree giving LOD = 3.1 with a parametric model, and a log Bayes Factor = 1.5 from a Bayesian oligogenic approach. Of the 293 SNPs spanning the implicated region on 4q, rs6829588 completely explained the evidence of linkage. This SNP accounted for 39% of the apoB phenotypic variance, with heterozygotes for this SNP having a trait value that was approximately 30% higher than that of the high-frequency homozygote, thus identifying and considerably refining a strong candidate region. These results illustrate the advantage of using large pedigrees in the search for rare variants: reduced genetic heterogeneity within single pedigrees coupled with the large number of individuals segregating otherwise-rare single variants leads to high power to implicate such variants.

La elevación del colesterol unido a lipoproteínas de alta densidad: perspectiva futura. La CETP como diana terapéutica

Cholesteryl ester transfer protein (CETP) facilitates transfer of neutral lipids between lipoprotein classes. CETP plays a key role in cholesterol homeostasis, especially in the redistribution of cholesterol among particles and in reverse cholesterol transport. Consequently, modifying the activity of this protein could influence the development and progression of atheromatosis. The effects of inhibiting CETP include reductions in lowdensity lipoprotein (LDL)-cholesterol and cholesterol in triglyceride-rich particles and increases in high-density lipoprotein (HDL)-cholesterol, apolipoprotein A-1 and the size of LDL and HDL particles. The induction of expression of CETP activity in mice increases susceptibility to atherosclerosis, while inhibition of CETP activity in rabbits tends to reduce its development. However, the role of CETP inhibition in atheromatosis in humans remains to be established.

Ethnic differences in serum lipoproteins and their determinants in South African women

The objective of the study was to characterize ethnic differences in lipid levels and low-density lipoprotein (LDL) particle size and subclasses in black and white South African women and to explore the associations with insulin sensitivity ( S I), body composition, and lifestyle factors. Fasting serum lipids and LDL size and subclasses, body composition (dual-energy x-ray absorptiometry), and S I (frequently sampled intravenous glucose tolerance test) were measured in normal-weight (body mass index <25 kg/m 2) black (n = 15) and white (n = 15), and obese (body mass index >30 kg/m 2) black (n = 13) and white (n = 13) women. Normal-weight and obese black women had lower triglycerides (0.59 ± 0.09 and 0.77 ± 0.10 vs 0.89 ± 0.09 and 0.93 ± 0.10 mmol/L, P < .05) and high-density lipoprotein cholesterol (1.2 ± 0.1 and 1.1 ± 0.1 vs 1.7 ± 0.1 and 1.6 ± 0.3 mmol/L, P < .01) than white women. The LDL particle size was not different, but obese black women had more LDL subclass IV (17.3% ± 1.0% vs 12.5% ± 1.0%, P < .01). In white women, triglycerides and LDL particle size correlated with S I ( P < .01), whereas cholesterol levels correlated with body fat ( P < .05). Low socioeconomic status, low dietary protein intake, and injectable contraceptive use were the major determinants of unfavorable lipid profiles in black women. Black women had lower triglyceride and high-density lipoprotein cholesterol levels and more small dense LDL particles than white women. The major determinants of serum lipids in black women were socioeconomic status and lifestyle factors, whereas in white women, S I and body composition most closely correlated with serum lipids.

Serum Folate and Low-Density Lipoprotein Particle Size

Nutritional parameters, such as B-vitamins, have not been studied for an association with low-density lipoprotein (LDL) particle size. The present study explored whether serum vitamin levels, including folate and vitamin B-12, could be associated with LDL particle size. Using a randomly selected population of 255 hospital workers, we collected detailed lipid profiles, including triglyceride (TG), high-density lipoprotein (HDL) cholesterol, and LDL particle sizes. The peak particle size of LDL was measured by density gradient ultracentrifugation and a pore gradient lipoprotein system. Serum folate and vitamin B-12 levels were measured about 1 year later and analyzed. Carotid intima-media thickness (IMT) and hepatic steatosis were diagnosed ultrasonographically, and metabolic syndrome was diagnosed using ATP III criteria. LDL peak particle size was significantly correlated with carotid mean IMT (r=-0.16, p=0.010). Serum folate levels were significantly and positively correlated with HDL cholesterol and negatively with TG, although the latter showed borderline significance. With increasing serum folate levels, the LDL peak particle size showed a gradual independent increase, even when adjusted for age, sex, hepatic steatosis, metabolic syndrome, and the TG/HDL cholesterol ratio. Folate may act to enhance LDL particle size. Future clinical and research work should include a study of the safe application and manipulation of folate levels in order to control LDL particle size.

Interleukin‐18 levels are associated with low‐density lipoproteins size

Both low-density lipoproteins (LDL) size and serum interleukin (IL)-18 levels have been shown to be predictors of cardiovascular morbidity and mortality. However, it is still unknown whether IL-18 levels are independently associated with LDL size. In this cross-sectional study including 53 premenopausal women (18-45 years), LDL size (by gradient gel electrophoresis), serum IL-18, high-sensitivity C-reactive protein (hs-CRP), serum lipids, insulin sensitivity (S(I), by frequently sampled intravenous glucose tolerance test) were measured. LDL size correlated with IL-18 (r = -0.38, P = 0.006), hs-CRP (r = -0.40, P = 0.003), S(I) (r = 0.36, P = 0.011), serum triglycerides (r = -0.32, P = 0.018) and high-density lipoproteins (HDL)-cholesterol (r = 0.40, P = 0.003). When these variables were entered into a regression model, serum IL-18 (beta = -0.26, P = 0.04), triglycerides (beta = -0.29, P = 0.02) and HDL-cholesterol (beta = 0.34, P = 0.01) levels were independently associated with LDL size, accounting for 42% of the variance (P < 0.001). Serum hs-CRP levels and S(I) were not significant independent predictors of LDL size in this model. This is the first report showing that elevated IL-18 levels are associated with reduced LDL size, independent of other inflammatory and metabolic risk factors. Future prospective studies are needed to evaluate the predictive role of IL-18 as an inflammatory marker of LDL size and the development of subclinical and/or clinical atherosclerosis.

Unfavorable lipid profile in women with endometriosis

Similar to dyslipidemia, the oxidative stress and intrinsic inflammatory status may be associated with the development of endometriosis. Thus, we performed a cross-sectional study and found that women with endometriosis had an increased low-density lipoprotein (LDL) and non-high-density lipoprotein (HDL) cholesterol levels compared with controls presumably without endometriosis.