Postpartum Weight Retention is Associated with Elevated Ratio of Oxidized LDL Lipids to HDL-Cholesterol

Oxidized LDL lipids (ox‐LDL) are associated with lifestyle diseases such as cardiovascular diseases, metabolic syndrome and type 2 diabetes. The present study investigated how postpartum weight retention effects on ox‐LDL and serum lipids. The study is a nested comparative research of a cluster‐randomized controlled trial, NELLI (lifestyle and counselling during pregnancy). During early pregnancy (8–12 weeks) and 1 year postpartum, 141 women participated in measurements for determining of plasma lipids: total cholesterol (T‐C), LDL‐cholesterol (LDL‐C), HDL‐cholesterol (HDL‐C), triacylglycerols (TAG) and ox‐LDL. Subjects were stratified into tertiles (weight loss, unaltered weight and weight gain groups) based on their weight change from baseline to follow‐up. Ox‐LDL was determined by baseline level of conjugated dienes in LDL lipids. Among the group of weight gainers, concentration of TAG reduced less (?0.14 vs. ?0.33, p = 0.002), HDL‐C reduced more (?0.31 vs. ?0.16, p = 0.003) and ox‐LDL/HDL‐C ratio increased (3.0 vs. ?0.2, p = 0.003) when compared to group of weight loss. Both T‐C and LDL‐C elevated more (0.14 vs. ?0.21, p = 0.008; 0.31 vs. 0.07, p = 0.015) and TAG and ox‐LDL reduced less (?0.33 vs. 0.20, p = 0.033; ?3.33 vs. ?0.68, p = 0.026) in unaltered weight group compared to weight loss group. The women who gained weight developed higher TAG and ox‐LDL/HDL‐C ratio as compared to those who lost weight. Postpartum weight retention of 3.4 kg or more is associated with atherogenic lipid profile.     

Increased HDL Size and Enhanced Apo A-I Catabolic Rates Are Associated With Doxorubicin-Induced Proteinuria in New Zealand White Rabbits

The catabolism and structure of high‐density lipoproteins (HDL) may be the determining factor of their atheroprotective properties. To better understand the role of the kidney in HDL catabolism, here we characterized HDL subclasses and the catabolic rates of apo A‐I in a rabbit model of proteinuria. Proteinuria was induced by intravenous administration of doxorubicin in New Zealand white rabbits (n = 10). HDL size and HDL subclass lipids were assessed by electrophoresis of the isolated lipoproteins. The catabolic rate of HDL‐apo A‐I was evaluated by exogenous radiolabelling with iodine‐131. Doxorubicin induced significant proteinuria after 4 weeks (4.47 ± 0.55 vs. 0.30 ± 0.02 g/L of protein in urine, P < 0.001) associated with increased uremia, creatininemia, and cardiotoxicity. Large HDL2b augmented significantly during proteinuria, whereas small HDL3b and HDL3c decreased compared to basal conditions. HDL2b, HDL2a, and HDL3a subclasses were enriched with triacylglycerols in proteinuric animals as determined by the triacylglycerol‐to‐phospholipid ratio; the cholesterol content in HDL subclasses remained unchanged. The fractional catabolic rate (FCR) of [¹³¹I]‐apo A‐I in the proteinuric rabbits was faster (FCR = 0.036 h^?1) compared to control rabbits group (FCR = 0.026 h^?1, P < 0.05). Apo E increased and apo A‐I decreased in HDL, whereas PON‐1 activity increased in proteinuric rabbits. Proteinuria was associated with an increased number of large HDL2b particles and a decreased number of small HDL3b and 3c. Proteinuria was also connected to an alteration in HDL subclass lipids, apolipoprotein content of HDL, high paraoxonase‐1 activity, and a rise in the fractional catabolic rate of the [¹³¹I]‐apo A‐I.     

Lipid Transfer to HDL is Higher in Marathon Runners than in Sedentary Subjects,but is Acutely Inhibited During the Run

Although exercise increases HDL-cholesterol, exercise-induced changes in HDL metabolism have been little explored. Lipid transfer to HDL is essential for HDL’s role in reverse cholesterol transport. We investigated the effects of acute exhaustive exercise on lipid transfer to HDL. We compared plasma lipid, apolipoprotein and cytokine levels and in vitro transfer of four lipids from a radioactively labeled lipid donor nanoemulsion to HDL in sedentary individuals (n = 28) and in marathon runners (n = 14) at baseline, immediately after and 72 h after a marathon. While HDL-cholesterol concentrations and apo A1 levels were higher in marathon runners, LDL-cholesterol, apo B and triacylglycerol levels were similar in both groups. Transfers of non-esterified cholesterol [6.8 (5.7–7.2) vs. 5.2 (4.5–6), p = 0.001], phospholipids [21.7 (20.4–22.2) vs. 8.2 (7.7–8.9), p = 0.0001] and triacylglycerol [3.7 (3.1–4) vs. 1.3 (0.8–1.7), p = 0.0001] were higher in marathon runners, but esterified-cholesterol transfer was similar. Immediately after the marathon, LDL- and HDL-cholesterol concentrations and apo A1 levels were unchanged, but apo B and triacylglycerol levels increased. Lipid transfer of non-esterified cholesterol [6.8 (5.7–7.2) vs. 5.8 (4.9–6.6), p = 0.0001], phospholipids [21.7 (20.4–22.2) vs. 19.1 (18.6–19.3), p = 0.0001], esterified-cholesterol [3.2 (2.2–3.8) vs. 2.3 (2–2.9), p = 0.02] and triacylglycerol [3.7 (3.1–4) vs. 2.6 (2.1–2.8), p = 0.0001] to HDL were all reduced immediately after the marathon but returned to baseline 72 h later. Running a marathon increased IL-6 and TNF-α levels, but after 72 h these values returned to baseline. Lipid transfer, except esterified-cholesterol transfer, was higher in marathon runners than in sedentary individuals, but the marathon itself acutely inhibited lipid transfer. In light of these novel observations, further study is required to clarify how these metabolic changes can influence HDL composition and anti-atherogenic function.     

Aerobic Training in Young Men Increases the Transfer of Cholesterol to High Density Lipoprotein In Vitro: Impact of High Density Lipoprotein Size

Exercise training not only improves the plasma lipid profile but also reduces risk of developing coronary heart disease. We investigate whether plasma lipids and high density lipoprotein (HDL) metabolism are affected by aerobic training and whether the high-density lipoprotein cholesterol (HDL-C) levels at baseline influence exercise-induced changes in HDL. Seventy-one male sedentary volunteers were evaluated and allocated in two subgroups, according to the HLD-C levels (< or >40 mg/dL). Participants underwent an 18-week aerobic training period. Blood was sampled before and after training for biochemical analysis. Plasma lipids, apolipoproteins, HDL diameter, and VO₂ peak were determined. Lipid transfers to HDL were determined in vitro by incubating plasma samples with a donor lipid artificial nanoemulsion. After the 18-week period of aerobic training, the VO₂ peak increased, while the mean body mass index (BMI) decreased. HDL-C concentration was higher after the training period, but low-density lipoprotein cholesterol (LDL-C) and non-HDL-C did not change. The transfer of esterified cholesterol and phospholipids was greater after exercise training, but the triacylglycerol and unesterified cholesterol transfers were unchanged. The HDL particle diameter increased after aerobic training in all participants. When the participants were separated in low-HDL and normal-HDL groups, the postaerobic exercise increment in HDL-C was higher in the low-HDL group, while the transfer of esterified cholesterol was lower. In conclusion, aerobic exercise training increases the lipid transfers to HDL, as measured by an in vitro method, which possibly contributes to the classical elevation of the HDL-C associated with training.     

Plasma Phospholipid Fatty Acid Profile is Altered in Both Septic and Non-Septic Critically Ill: A Correlation with Inflammatory Markers and Albumin

This study analyzes fatty acid (FA) composition in plasma lipids and erythrocyte phospholipids while comparing septic and non‐septic critically ill patients. The aim was to describe impacts of infection and the inflammatory process. Patients with severe sepsis (SP, n = 13); age‐, sex‐ and APACHE II score‐matched non‐septic critically ill with systemic inflammatory response syndrome (NSP, n = 13); and age‐/sex‐matched healthy controls (HC, n = 13) were included in a prospective case–control study during the first 24 h after admission to the intensive care unit. In both SP and NSP, lower n‐6 polyunsaturated FA (PUFA) accompanied by higher proportions of monounsaturated FA (MUFA) in plasma phospholipids (PPL) was observed relative to HC. MUFA proportion was negatively correlated with n‐6 PUFA, high density lipoprotein cholesterol (HDL‐C), and albumin. MUFA was positively correlated with C‐reactive protein (CRP), procalcitonin (PCT), interleukins (IL‐6, IL‐10), oxidized low density lipoproteins (ox‐LDL), and conjugated dienes (CD). In both SP and NSP, inflammatory and lipid peroxidation markers were significantly higher—CRP (p < 0.001; p = 0.08), IL‐6, IL‐10, TNF‐α (p < 0.01, p = 0.06), ox‐LDL, and CD while total cholesterol, HDL‐C, LDL‐C albumin, and 20:4n‐6/22:6n‐3 and n‐6/n‐3 ratios were lower compared to HC. In conclusion, the changes in plasma lipid FA profile relate to the intensity of inflammatory and peroxidative response regardless of insult etiology. The lower MUFA and higher n‐6 PUFA proportions in PPL were inversely correlated with cholesterol and albumin levels.     

Phospholipid Transfer Protein Deficiency Decreases the Content of S1P in HDL via the Loss of its Transfer Capability

Sphingosine‐1‐phosphate (S1P) is an amphiphilic signaling molecule, which is enriched in functional high density lipoprotein (HDL) and shows arterial protection. The distribution of S1P is changed with increased plasma phospholipid transfer protein (PLTP) activity and impaired HDL function in patients with coronary heart diseases. Therefore, we hypothesized that PLTP might transfer S1P among cells or lipoproteins. We found that plasma S1P contents were decreased by 60.1 % in PLTP knockout mice (PLTP?/?, N = 5) compared with their wild type littermates (WT, N = 5) (151.70 ± 38.59 vs. 379.32 ± 59.90 nmol/l, P<0.01). S1P content in HDL fraction (HDL‐S1P) from PLTP?/? was decreased by 64.7 % compared with WT (49.36 ± 1.49 vs. 139.76 ± 2.94 nmol/l, P<0.01). The results of the S1P transfer assay indicated that PLTP could facilitate S1P transport from erythrocytes to HDL at 37 °C in D‐Hanks buffer. Plasma content of apolipoprotein M, a specific adaptor of S1P, was not changed in PLTP?/? compared with WT. Therefore, we concluded that PLTP was a key factor to maintain plasma HDL‐S1P, and PLTP deficiency could decrease the S1P content in plasma lipoproteins, which involves its capability of transferring S1P from erythrocyte to HDL.     

Treatment of Low HDL‐C Subjects with the CETP Modulator Dalcetrapib Increases Plasma Campesterol Only in Those Without ABCA1 and/or ApoA1 Mutations

We investigated the effect of dalcetrapib treatment on phytosterol levels in patients with familial combined hyperlipidemia (FCH) or familial hypoalphalipoproteinemia (FHA) due to mutations in apolipoprotein A1 (ApoA1) or ATP‐binding cassette transporter A1 (ABCA1). Patients (n = 40) with FCH or FHA received dalcetrapib 600 mg or placebo in this 4‐week, double‐blind, crossover study. Lipids, apolipoproteins, cholesteryl ester transfer protein (CETP) activity and mass, and phytosterols were assessed. Dalcetrapib increased high‐density lipoprotein cholesterol (HDL‐C) and ApoA1 levels to a similar extent in FHA (+22.8, +13.9 %) and FCH (+18.4, +12.1 %), both p < 0.001 vs. placebo. Changes in CETP activity and mass were comparable for FHA (?31.5, +120.9 %) and FCH (?26.6, +111.9 %), both p < 0.0001 vs. placebo. Campesterol and lathosterol were unchanged in FHA (+3.8, +3.0 %), but only campesterol was markedly increased in FCH (+25.0 %, p < 0.0001 vs. placebo). Campesterol increased with dalcetrapib treatment in FCH but not in FHA, despite comparable HDL‐C and ApoA1 increases, suggesting that ApoA1 and/or ABCA1 is essential for HDL lipidation by enterocytes in humans.     

Occurrence of dyslipidemia in spontaneous intracerebral hemorrhage

Background: Dyslipidemia, mainly hypocholesterolemia is considered to be a risk factor (RF) for spontaneous intracerebral hemorrhage (SICH). The aim of our study was to assess its role in our SICH patients. Methods: In a hospital‐based cross‐section study, laboratory assessments of total cholesterol (TC), triglycerides (TG), high‐density cholesterol (HDL‐C) and low‐density cholesterol (LDL‐C) plasma levels were performed in 80 SICH patients without vascular malformation and in a control group (CG) of 80 age‐ and sex‐matched patients with low back pain. All patients were treated at the Departments of Neurology and Neurosurgery, University Hospital, Olomouc, Czech Republic. Two‐sample t‐test and Mann‐Whitney test were applied when assessing statistical significance. Results: The following mean lipid plasma levels were found in SICH patients versus CG subjects (in mmol/L): TC, 5.89 vs. 5.48 (p = 0.007); TG, 1.31 vs. 2.10 (p <0.0001); HDL‐C, 1.58 vs. 1.33 (p = 0.0001); LDL‐C, 3.70 vs. 3.18 (p = 0.0004). Conclusions: TC and LDL‐C plasma levels were higher in SICH patients in the Olomouc region of the Czech Republic.     

High Density Lipoprotein Level is Negatively Associated With the Increase of Oxidized Low Density Lipoprotein Lipids After a Fatty Meal

Recent reports show that a fatty meal can substantially increase the concentration of oxidized lipids in low density lipoprotein (LDL). Knowing the LDL‐specific antioxidant effects of high density lipoprotein (HDL), we aimed to investigate whether HDL can modify the postprandial oxidative stress after a fatty meal. Subjects of the study (n = 71) consumed a test meal (a standard hamburger meal) rich in lipid peroxides, and blood samples were taken before, 120, 240, and 360 min after the meal. The study subjects were divided into four subgroups according to the pre‐meal HDL cholesterol value (HDL subgroup 1, 0.66–0.91; subgroup 2, 0.93–1.13; subgroup 3, 1.16–1.35; subgroup 4, 1.40–2.65 mmol/L). The test meal induced a marked postprandial increase in the concentration of oxidized LDL lipids in all four subgroups. The pre‐meal HDL level was associated with the extent of the postprandial rise in oxidized LDL lipids. From baseline to 6 h after the meal, the concentration of ox‐LDL increased by 48, 31, 24, and 16 % in the HDL subgroup 1, 2, 3, and 4, respectively, and the increase was higher in subgroup 1 compared to subgroup 3 (p = 0.028) and subgroup 4 (p = 0.0081), respectively. The pre‐meal HDL correlated with both the amount and the rate of increase of oxidized LDL lipids. Results of the present study show that HDL is associated with the postprandial appearance of lipid peroxides in LDL. It is therefore likely that the sequestration and transport of atherogenic lipid peroxides is another significant mechanism contributing to cardioprotection by HDL.     

CETP and LCAT Gene Polymorphisms Are Associated with High‐Density Lipoprotein Subclasses and Acute Coronary Syndrome

We evaluated whether CETP and LCAT gene polymorphisms are statistically associated with the high‐density lipoprotein (HDL) size distribution, the cholesterol level of HDL subclasses, and the acute coronary syndrome (ACS) susceptibility. Two CETP gene polymorphisms (rs4783961 and rs708272) and one LCAT polymorphism (rs2292318) were genotyped by 5′ exonuclease TaqMan assays in 619 patients with ACS and 607 control individuals. For HDL analysis, a subgroup of 100 healthy individuals was recruited; the HDL subclasses were separated via ultracentrifugation and polyacrylamide gradient gel electrophoresis under native conditions. Under a dominant model, the G allele of the rs708272 polymorphism was associated with an increased risk of ACS (odds ratios [OR] = 1.45, corrected p‐value [pC_Dom] = 0.036). The linkage disequilibrium analysis showed that one of the eight possible combinations was associated with the risk of developing ACS (OR = 1.52, pC = 0.02), which suggests that it may contribute to coronary atherosclerosis. The rs708272 G allele carriers had a lower concentration of cholesterol associated with the HDL2a and HDL3a subclasses when compared with subjects carrying the A allele. Carriers of LCAT rs2292318 A allele showed a lower concentration of high‐density lipoprotein‐cholesterol (HDL‐C) in comparison to the GG genotype; the cholesterol associated with the each one of the five HDL subclasses was significantly lower in rs2292318 A than in GG subjects. In summary, this study demonstrates that the rs708272 polymorphism is associated with a heightened risk of developing ACS. In addition, we report the association of the rs708272 and rs2292318 polymorphisms with HDL‐C levels and HDL subclasses.     

The effect of dietary n−3 polyunsaturated fatty acids on HDL cholesterol in Chukot residentsvs muscovites

Native Chukot Peninsula residents, in contrast to Muscovites, consume a diet rich in n−3 polyunsaturated fatty acids. This dietary peculiarity is reflected in differences in plasma lipid and apolipoprotein contents. The Chukot residents have lower contents of total cholesterol, triglyceride, LDL (low density lipoprotein) cholesterol and apolipoprotein B, but higher HDL (high density lipoprotein) cholesterol levels than do Muscovites. The apolipoprotein A-I levels were identical in both groups. A higher HDL cholesterol to apolipoprotein A-I ratio was determined in the coastline Chukot residents (0.52±0.01) than in Muscovites (0.43±0.01; p<0.01). In contrast to Muscovites, the coastline Chukot residents also had higher n−3 and lower n−6 polyunsaturated fatty acid percentages in plasma and erythrocyte lipids, and lower phosphatidylcholine and higher sphingomyelin or phosphatidylethanolamine levels in HDL_2b and HDL₃. The higher HDL cholesterol levels in the plasma of the coastline Chukot residents appears to reflect the higher cholesterol-scavenging capacity of their HDL. We conclude from this study that the regular consumption of dietary n−3 polyunsaturated fatty acids by the coastline Chukot residents decreased LDL cholesterol transfer from plasma to peripheral cells, and enhanced cholesterol efflux from cellular membranes toward HDL.     

Fat Distribution and Lipid Profile of Young Adults with Congenital Adrenal Hyperplasia Due to 21-Hydroxylase Enzyme Deficiency

We aimed to compare detailed fat distribution and lipid profile between young adults with congenital adrenal hyperplasia due to 21-hydroxylase enzyme deficiency and a control group. We also verified independent associations of treatment duration and daily hydrocortisone dose equivalent (HDE) with lipid profile within patients. This case–control study included 23 patients (7 male and 16 female) matched by an age range of young adults (18–31 years) with 20 control subjects (8 male and 12 female). Dual energy X-ray absorptiometry was used to measure the fat distribution. Male patients demonstrated elevated indices of fat mass for total (7.7 ± 2.1 vs. 4.5 ± 1.3 kg/m², p = 0.003), trunk (4.0 ± 1.2 vs. 2.2 ± 0.8 kg/m², p = 0.005), android (0.63 ± 0.24 vs. 0.32 ± 0.15 kg/m², p = 0.008), gynoid (1.34 ± 0.43 vs. 0.74 ± 0.24 kg/m², p = 0.005), arm (0.65 ± 0.16 vs. 0.39 ± 0.10 kg/m², p = 0.009), and leg regions (2.7 ± 0.8 vs. 1.6 ± 0.4 kg/m², p = 0.005) than the control group, but not in females. However, female patients demonstrated elevated ratio of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol (1.90 ± 0.46 vs. 1.39 ± 0.47, p = 0.009) than the control group, but not in males. Total fat mass was inversely correlated with total testosterone (r = −0.64, p = 0.014) and positively correlated with leptin in males (r = 0.75, p = 0.002). An elevated daily HDE (β = 0.43, p = 0.038 and β = 0.47, p = 0.033) and trunk to total fat mass ratio (β = 0.46, p = 0.025, and β = 0.45, p = 0.037) were independently correlated with impaired lipid profile markers. Although there is no altered lipid profile, male patients demonstrated an increased fat distribution. However, female patients presented with an impaired lipid profile marker but demonstrated close values of normal fat distribution. Interestingly, the dose of glucocorticoid therapy can have some role in the lipid mechanisms.     

Higher levels of plasma cholesterol sulfate in patients with liver cirrhosis and hypercholesterolemia

An analytical method for the determination of cholesterol sulfate (CS) in plasma using gas-liquid chromatography was developed. We measured plasma CS concentrations in patients with liver cirrhosis and hypercholesterolemia as examples of disorders that involve aberrations in cholesterol metabolism. Patients with liver cirrhosis had plasma CS concentrations that were significantly higher than those of control subjects (444.6±51.7vs. 253.0±24.6 μg/dL, mean ±SE). The levels of other lipids were lower in cirrhotics, although the differences were not significant. There was no correlation between the levels of CS and sulfated bile acids in cirrhotic patients. CS levels in plasma were also higher in subjects with hypercholesterolemia (413.7±44.5 μg/gL) however, the ratio of CS to total cholesterol (TC) clearly differed between cirrhotics and hypercholesterolemic subjects (1.44±0.11×10⁻³,vs. 3.31 ±0.63×10⁻³;P<0.05). Both in subjects with hypercholesterolemia and in healthy controls, the CS/TC ratio was similar and CS accounted for roughly 0.14% of the TC concentration.     

Plasma Lipids,Lipoprotein Metabolism and HDL Lipid Transfers are Equally Altered in Metabolic Syndrome and in Type 2 Diabetes

Metabolic syndrome (MetS) refers to states of insulin resistance that predispose to development of cardiovascular disease and type 2 diabetes (T2DM). The aim was to investigate whether plasma lipids and lipid metabolism differ in MetS patients compared to those with T2DM with poor glycemic control (glycated hemoglobin > 7.0). Eighteen patients with T2DM, 18 with MetS and 14 controls, paired for age (40–70 years) and body mass index (BMI), were studied. Plasma lipids and the kinetics of a triacylglycerol-rich emulsion labeled with [³H]-triolein ([³H]-TAG) and [¹⁴C]-cholesteryl esters ([¹⁴C]-CE) injected intravenously followed by one-hour blood sampling were determined. Lipid transfers from an artificial nanoemulsion donor to high-density lipoprotien (HDL) were assayed in vitro. Low-density lipoprotein (LDL) and HDL cholesterol (mg/dl) were not different in T2DM (128 ± 7; 42 ± 7) and MetS (142 ± 6; 39 ± 3), but triacylglycerols were even higher in MetS (215 ± 13) than in T2DM (161 ±11, p < 0.05). Fractional clearance rate (FCR, in min¹) of [³H]-TAG and [¹⁴C]-CE were equal in T2DM (0.008 ± 0.018; 0.005 ± 0.024) and MetS (0.010 ± 0.016; 0.006 ± 0.013), and both were reduced compared to controls. The transfer of non-esterified cholesterol, phospholipids and triacylglycerols to HDL was higher in MetS and T2DM than in controls (p < 0.01). Cholesteryl ester transfer and HDL size were equal in all groups. Results imply that MetS is equal to poorly controlled T2DM concerning the disturbances of plasma lipid metabolism examined here, and suggest that there are different thresholds for the insulin action on glucose and lipids. These findings highlight the magnitude of the lipid disturbances in MetS, and may have implications in the prevention of cardiovascular diseases.     

Effect of grass vs. concentrate feeding on the fatty acid profile of different fat depots in lambs

The aim of this study was to produce high‐quality meat from lambs under different feeding conditions, as measured by the accumulation of n‐3 fatty acids and conjugated linoleic acids (CLA) in muscle and subcutaneous fat. In total, 13 male crossbred lambs (Black Head×Gotland), each at 24 kg live weight, were divided into two feeding groups. Lambs were kept either on pasture (pasture grazing, n = 6) or in the stable (concentrate feeding, n = 7). The linolenic acid (C18:3n‐3) contained in the grass was absorbed and deposited into the different lipid classes of muscle and subcutaneous fat. The proportion of total n‐3 fatty acids in the different lipids of grazing lambs was significantly (p = 0.05) higher compared to that in concentrate‐fed lambs. The n‐6/n‐3 ratio (mean ± SEM) in muscle of grazing lambs was 1.2 ± 0.09 in contrast to 2.3 ± 0.09 (p = 0.05) of the animals kept in the stable. In subcutaneous fat, this ratio was 0.9 ± 0.2 in lambs kept on pasture versus 3.5 ± 0.2 (p = 0.05) after indoor keeping. The relative concentration of C18:1trans‐11 in total muscle lipids, phospholipids, triacylglycerols and subcutaneous fat was significantly increased by grass feeding compared to concentrate feeding. Significant influences of feeding were shown for saturated fatty acids. In concentrate‐fed lambs, a lower content of saturated fatty acids was detected. The proportion of CLAcis‐9,trans‐11 (1.9 ± 0.2% vs. 1.1 ± 0.1% in muscle, 2.5 ± 0.2% vs. 1.4 ± 0.2% in subcutaneous fat, 0.7 ± 0.04% vs. 0.4 ± 0.04% in phospholipids) in lambs was significantly (p = 0.05) higher after grazing than after concentrate feeding, respectively.     

Relationships between Very Low-Density Lipoproteins–Ceramides, −Diacylglycerols,and –Triacylglycerols in Insulin-Resistant Men

This short report describes the relationships between concentrations of ceramides (CER), diacylglycerols (DAG), triacylglycerols (TAG) in very low-density lipoproteins (VLDL) particles, and hepatic lipid accumulation. VLDL particles were isolated from male subjects (n = 12, mean ± SD, age 42.1 ± 5.4 years, BMI 37.4 ± 4.1 kg/m², ALT 45 ± 21 U/L) and apolipoprotein B100 (apoB100), VLDL-TAG, -CER, and -DAG quantified. The contents of all three lipids were highly correlated with VLDL particle number (r ≥ 0.768, p ≤ 0.003). The molar quantity of VLDL-TAG was 3× that of DAG and 137× that of CER (14,053 ± 5714, 5004 ± 2714, and 105 ± 49 mol/mol apoB100, respectively). Reduced VLDL-CER concentrations were associated with both higher insulin levels (r = −0.645, p = 0.024) and intrahepatic-TAG (r = −0.670, p = 0.017). In fatty liver, the secretion of hepatic TAG, CER, and DAG may be suppressed and contribute to intrahepatic lipotoxicity. The mechanisms by which hepatic-CER and -DAG synthesis and assembly into VLDL is coordinately controlled with TAG will be important in understanding the emerging role of elevated CER contributing to cardiometabolic disease.     

<Emphasis Type="SmallCaps">l</Emphasis>-Carnitine/Simvastatin Reduces Lipoprotein (a) Levels Compared with Simvastatin Monotherapy: A Randomized Double-Blind Placebo-Controlled Study

Lipoprotein (a) [Lp(a)] is an independent risk factor for cardiovascular disease. There are currently limited therapeutic options to lower Lp(a) levels. l ‐Carnitine has been reported to reduce Lp(a) levels. The aim of this study was to compare the effect of l ‐carnitine/simvastatin co‐administration with that of simvastatin monotherapy on Lp(a) levels in subjects with mixed hyperlipidemia and elevated Lp(a) concentration. Subjects with levels of low‐density lipoprotein cholesterol (LDL‐C) >160 mg/dL, triacylglycerol (TAG) >150 mg/dL and Lp(a) >20 mg/dL were included in this study. Subjects were randomly allocated to receive l ‐carnitine 2 g/day plus simvastatin 20 mg/day (N = 29) or placebo plus simvastatin 20 mg/day (N = 29) for a total of 12 weeks. Lp(a) was significantly reduced in the l ‐carnitine/simvastatin group [?19.4%, from 52 (20–171) to 42 (15–102) mg/dL; p = 0.01], but not in the placebo/simvastatin group [?6.7%, from 56 (26–108) to 52 (27–93) mg/dL, p = NS versus baseline and p = 0.016 for the comparison between groups]. Similar significant reductions in total cholesterol, LDL‐C, apolipoprotein (apo) B and TAG were observed in both groups. Co‐administration of l ‐carnitine with simvastatin was associated with a significant, albeit modest, reduction in Lp(a) compared with simvastatin monotherapy in subjects with mixed hyperlipidemia and elevated baseline Lp(a) levels.     

Effect of extra virgin olive oil on glycaemia in healthy young subjects

In this approach we studied the glycaemia levels in 20 healthy young volunteers (26 ± 2 years), before and after a 30‐day intake of 50 mL of extra virgin olive oil (EVOO). We selected an oil rich in phenolic compounds (523 mg/L) with a high content of secoiridoidic derivatives (over 94.5%). The findings from our study reveal a significant decrease of glycaemia from 89.6 ± 6.8 to 82.7 ± 10.3 mg/dL (p<0.05), related to a long term daily intake of the study EVOO, as the only added fat. A significant increment of the HDL cholesterol, from 68.7 ± 11.5 to 75.2 ± 4.9 mg/dL, was also highlighted. Total cholesterol, LDL, VLDL, triglycerides, and blood pressure did not show significant variation after the 30‐day consumption of this EVOO. So far, few articles have described the influence of EVOO consumption, on plasma glucose levels in humans. This effect is observed in a group of healthy young humans. Moreover, we confirm that the level of free hydroxytyrosol (OH‐Tyr) in plasma increased up to fourfold (p<0.05) after the 30‐day intake of this EVOO. In addition, the excretion in urine of the main metabolite of OH‐Tyr, homovanillic acid (HVA), significantly increased.     

Diminished macrophage cholesterol removal rate by the altered HDL metabolism in the Nagase analbuminemic rat

Dyslipoproteinemia of the Nagase analbuminemic rat (NAR) is characterized by elevated concentrations of VLDL and LDL attributed to increased rates of liver lipoprotein synthesis. Increased lysophosphatidylcholine (LPC) in NAR HDL has been attributed to high plasma LCAT activity. We show here that, as compared with Sprague-Dawley rats (SDR), NAR plasma triacylglycerol (TAG), total cholesterol (TC), HDL TAG, protein, total phospholipids (PL), LPC, and PS are increased. These alterations rendered the NAR HDL particle more susceptible to the activity of the enzyme hepatic lipoprotein lipase (HL), which otherwise was unaltered in our study. Fractional catabolic rates in blood of the autologous ¹²⁵I-apoHDL (median and lower quartile values), were, respectively, 0.231 and 1.645 (n=10) in NAR as compared with 0.140 and 0.109 (n=10) in SDR (P=0.012), corresponding to synthesis rates of HDL protein of 89.8±33.7 mg/d in NAR and 17.4±6.5 mg/d in SDR (P=0.0122). Furthermore, Swiss mouse macrophage free-cholesterol (FC) efflux rates, measured as the percent [¹⁴C]-cholesterol efflux/6 h, were 8.2±2.3 (n=9) in NAR HDL and 11.2±3.2 (n=10) in SDR HDL (P=0.03). Therefore, in NAR the modification of the HDL composition slows down the cell FC efflux rate, and together with the increased rate of plasma HDL metabolism influences the reverse cholesterol transport system.     

Vitamin D and Evening Primrose Oil Administration Improve Glycemia and Lipid Profiles in Women with Gestational Diabetes

Limited data are available assessing the effects of vitamin D and evening primrose oil (EPO) administration on markers of insulin resistance and lipid concentrations in gestational diabetes mellitus (GDM). This study was designed to evaluate the effects of vitamin D and EPO administration on insulin resistance and lipid concentrations among women with GDM. In this prospective randomized, double‐blind, placebo‐controlled clinical trial, 60 participants with GDM were divided into 2 groups of either 1000 IU vitamin D3 and 1000 mg EPO or placebo for 6 weeks. At the beginning and end of the study, fasting blood samples were obtained from the participants to measure related variables. After 6 weeks of intervention, changes in fasting plasma glucose (?3.6 ± 7.5 vs. +1.5 ± 11.4 mg/dL, P = 0.04), serum insulin concentrations (?2.0 ± 5.3 vs. +4.6 ± 10.7 µIU/mL, P = 0.004), homeostasis model of assessment (HOMA) insulin resistance (?0.5 ± 1.1 vs. +1.1 ± 2.5, P = 0.003), HOMA‐B cell function (?7.7 ± 23.3 vs. +17.4 ± 42.9, P = 0.007) and the quantitative insulin sensitivity check index (+0.01 ± 0.02 vs. ?0.01 ± 0.02, P = 0.007) in the vitamin D plus EPO group were significantly different from the placebo group. In addition, compared with the placebo, vitamin D and EPO supplementation resulted in significant reductions in serum TAG (?20.0 ± 54.3 vs. +34.3 ± 38.2 mg/dL, P < 0.001), VLDL (?4.0 ± 10.9 vs. +6.9 ± 7.6 mg/dL, P < 0.001), TC (?22.1 ± 32.6 vs. +5.3 ± 20.1 mg/dL, P < 0.001), LDL concentrations (?18.0 ± 25.5 vs. +1.8 ± 15.7 mg/dL, P = 0.001) and TC/HDL (?0.3 ± 0.4 vs. +0.3 ± 0.5 mg/dL, P < 0.001). We did not observe any significant effect of vitamin D and EPO supplementation on serum HDL concentrations. Clinical trial registration number: http://www.irct.ir : IRCT201509115623N52.