Density Lipoprotein Subfractions Research Articles

P-087: Effect of changing the type of fat on markers of cardiometabolic risk in obese rat

Background The purpose of this study is to verify if replacing margarine by sardine oil attenuates lipid peroxidation and improves reverse cholesterol transport in obese rats. Methods Obesity was induced by feeding a high-fat-diet during 3 months. At 400 ± 10 g the obese rats (n = 24) were divided into 2 groups and consumed during 1 month (d30) 20% margarine or sardine oil. At d30, 6 rats from each group were sacrificed and the remaining rats were then subjected to a change in diet for 1 month (d60): margarine was replaced by sardine oil and inversely. Results The substitution of sardine oil by margarine enhanced cholesterol -very low density lipoprotein (C-VLDL) (+21%) and C-low density lipoprotein (LDL-HDL1) (+17%) and decreased C-high density lipoprotein (HDL2 and HDL3) subfractions by 38% and 15%, respectively. Indeed, lipid peroxidation was enhanced in LDL-HDL1 (+26%) and HDL2 and HDL3 (+41%). When margarine was replaced by sardine oil, C-VLDL, C-LDL-HDL1, C-HDL2 concentrations were deceased by –58, –81 and –35%, respectively and lecithin: cholesterol acyltransferase (LCAT) activity was significantly higher (+74%). Indeed, HDL2 and HDL3 lipid peroxidation was decreased respectively by 28% and 14%. Conclusions In obese rats, the replacement of sardine oil by margarine seems to increase atherogenic markers and lipoperoxidation and consequently seemed to enhance cardiovascular diseases. However, the substitution of margarine by sardine oil can reduce lipid peroxidation and improves reverse cholesterol transport by increasing the activity of LCAT and thus ensuring a fortification in HDL2 cholesteryl esters. Sardine oil compared to margarine may have a protective effect against cardiovascular risk by improving the anti-atherogenic metabolic pathway of cholesterol.

LOW-DENSITY LIPOPROTEIN SUBFRACTIONS AND VARYING DEGREE OF CORONARY STENOSIS

Aim.To investigate whether low and intermediate density lipoprotein (LDL, IDL) subfractions are associated with a degree of angiographically verified coronary atherosclerosis, as well as with other biochemical risk factors of coronary heart disease (CHD), and hypertriglyceridemia (HTG) in particular.Material and methods.The study included 129 patients (76 men and 53 women), aged 33–75 years, who were referred for coronary angiography. All participants were divided into three groups by the degree of coronary artery (CA) stenosis: 0–20%, 21–70%, and >70%. LDL and IDL subfractions were measured with the Lipoprint LDL System (electrophoresis in 3% polyacrylamide gel).Results.All groups were similar by the levels of lipid and apoprotein parameters. The levels of high-sensitive C-reactive protein and glucose, as well as HOMA-IR index, were higher in Group 3 patients. In most cases of severe CA stenosis, small dense LDL particles were detected. In HTG patients, higher levels of small dense LDL3 particles were registered only together with the CA stenosis of at least 21–70%.Conclusion.The findings on lipoprotein subfractions, obtained with the Lipoprint LDL System, have demonstrated that in patients with verified coronary atherosclerosis, there is a link between the levels of more atherogenic small dense LDL3 particles, the degree of CA stenosis, and blood TG levels. The combination of HTG and high LDL3 levels could be considered an additional marker of severe CA atherosclerosis.

4P-1012 Quick and sensitive monitoring of oxidatively modified low density lipoprotein (LDL) subfractions by capillary isotachophoresis (cITP)

4P-1012 Quick and sensitive monitoring of oxidatively modified low density lipoprotein (LDL) subfractions by capillary isotachophoresis (cITP)

Pioglitazone reduces atherogenic dense low density lipoprotein (LDL) particles in patients with type 2 diabetes mellitus

Aim The new oral antidiabetic agent pioglitazone improves insulin sensitivity and glycaemic control, lowers triglycerides and increases high density lipoprotein (HDL) cholesterol in type 2 diabetes. The effect of pioglitazone on low density lipoprotein (LDL) subfractions is investigated, herein. Methods The effect of pioglitazone monotherapy (45 mg o.d. for six months) on LDL subfractions was observed in 30 patients with poorly controlled type 2 diabetes (HbA1C ≥ 7.5% and < 11.5% and triglycerides ≥ 150 mg/dL). The distribution of LDL subfractions was determined by equilibrium density gradient ultracentrifugation before and during treatment. Results HbA1C (9.5% before and 7.4% on treatment, p<0.001), triglycerides (-135 mg/dL [-32.2%], p=0.002) and apo B in LDL-6 (the most dense LDL subfraction) decreased significantly. The mean diameter of LDL particles increased (19.5 nm before and 19.8 nm on treatment, p=0.005), while the mean LDL density decreased significantly (from 1.0394 kg/L to 1.0381 kg/L on treatment; p=0.033). HDL increased from 36.3 mg/dL to 44.2 mg/dL (+ 21.6%, p<0.001). Total cholesterol and LDL-cholesterol did not change significantly. Conclusions The results confirm that pioglitazone improves glycaemic control in patients with type 2 diabetes. In addition, pioglitazone reduced the proportion of atherogenic dense LDL. The effects of pioglitazone on lipoprotein metabolism may translate into a reduced risk for atherosclerotic complications in type 2 diabetes.

Association of Atherogenic Low Density Lipoprotein (Ldl) Subfractions with Carotid Atherosclerosis

Association of Atherogenic Low Density Lipoprotein (Ldl) Subfractions with Carotid Atherosclerosis

1.P.2 Crystallization and preliminary X-ray diffraction data of two different human low density lipoprotein (LDL) subfractions

1.P.2 Crystallization and preliminary X-ray diffraction data of two different human low density lipoprotein (LDL) subfractions

Is there a menopausal metabolic syndrome?

Estradiol-17β has beneficial effects on a range of metabolic risk factors for coronary heart disease and the decline in estrogen concentrations at the menopause would be expected to have adverse effects. Review of the literature on effects of the menopause and of estradiol-17β provides evidence for the following changes occuring at or after the menopause: increased total cholesterol and triglycerides; decreased high density lipoprotein (HDL) and HDL subfraction 2; increased low density lipoprotein, particularly in the small, dense subfraction; increased lipoprotein (a); increased insulin resistance; decreased insulin secretion; decreased insulin elimination; increased android fat distribution; impaired vascular function; increased factor VII and fibrinogen, and reduced sex-hormone binding globulin. Many of these changes will themselves have adverse effects on other metabolic risk factors. This complex of inter-correlated adverse changes in metabolic risk factors justifies identification of a distinct menopausal metabolic syndrome which originates in estrogen deficiency and which could contribute to the increased risk of coronary heart disease seen in postmenopausal women. Estrogen replacement can diminish the expression of this syndrome.

Oxidative modification of low density lipoprotein (LDL) subfractions as measured by fluorescence spectroscopy

Oxidative modification of low density lipoprotein (LDL) subfractions as measured by fluorescence spectroscopy

Effects of nicotinic acid on serum cholesterol concentrations of high density lipoprotein subfractions HDL2, and HDL3, in hyperlipoproteinaemia

Nicotinic acid was given in a 4-g daily dose for 6 weeks to 41 weight-stable patients of mean age (+/- SD) 52 +/- 9 years, with type IIa, type IIb or type IV hyperlipoproteinaemia (HLP), in order to study its effects on serum cholesterol concentrations of high density lipoprotein (HDL) subfractions HDL2 and HDL3. The triglyceride and cholesterol levels of serum very low density (VLDL) and low density (LDL) lipoproteins decreased during treatment (P less than 0.001). Serum HDL and HDL2 cholesterol levels increased by 37% and 135%, respectively. These changes were positively correlated (r = 0.93; P less than 0.001). There was no significant change in mean serum HDL3 cholesterol concentration. A negative correlation existed between changes in HDL3 and HDL2 cholesterol levels (r = -0.54; P less than 0.001). Multiple stepwise linear regression analyses revealed that the initial HDL3 cholesterol predicted more than 30% of the increase in HDL2 cholesterol. Changes in the concentrations of HDL2 and HDL3 cholesterol after 6 weeks of drug treatment were not related to the type of HLP, neither were these effects of nicotinic acid correlated with changes in VLDL or LDL lipid levels. The concept has previously been proposed, on the basis of in vitro data, that HDL2 is formed from HDL3 particles in the blood. Our results suggest that, in man, this reaction is stimulated in vivo by prolonged nicotinic acid therapy.

High-density lipoprotein subfractions, apolipoproteins and antipyrine clearance in normal subjects

Serum high density lipoprotein (HDL) subfractions HDL2 and HDL3, apolipoproteins, and plasma antipyrine clearance (AP-CL) rate, an index of liver microsomal enzyme activity, were determined in 21 healthy subjects. High HDL cholesterol and HDL2 cholesterol concentrations and HDL cholesterol/cholesterol and HDL2/HDL3 cholesterol ratios were associated with high AP-CL. Phenobarbital enhanced antipyrine elimination and increased the apolipoprotein A-I/A-II ratio. Subjects who had high AP-CL had a more antiatherogenic HDL subfraction and apolipoprotein profile than those with low AP-CL.

Effects of age and physical performance capacity on distribution and composition of high-density lipoprotein subfractions in men

The influences of age and maximal aerobic capacity (VO2max) on serum lipoproteins with special regard to the concentration, composition and distribution of high density lipoprotein (HDL) subfractions were investigated in 51 healthy males of different characteristics: younger than 35 years, untrained (n = 14, mean age 28.2 years, SD 6.0; VO2max, 47.9 ml.kg-1.min-1, SD 5.8) and trained (n = 11, mean age 27.9 years, SD 4.3; VO2max, 61.1 ml.kg-1.min-1, SD 5.1), older than 50 years untrained (n = 14, mean age 58.9 years, SD 5.9, VO2max, 29.3 ml.kg-1.min-1, SD 5.3) and trained (n = 12, mean age 59.3 years, SD 7.2, VO2max, 45.7 ml.kg-1.min-1, SD 7.7). The fasting-state serum concentrations of total cholesterol, tri-acylglycerol and lipoprotein-cholesterol were measured. The HDL-subfractions were separated by density (rho) gradient ultracentrifugation. Concentrations of cholesterol, cholesterylester, tri-acylglycerol, phospholipids, apolipoprotein (apo) A-I and A-II were measured in the subfractions HDL2b: rho = 1.063-1.100 g.ml-1; HDL2al: rho = 1.00-1.110 g.ml-1; HDL2a2: rho = 1.110-1.150 g.ml-1; HDL3: rho = 1.150-1.210 g.ml-1. Elderly untrained subjects showed increased serum concentrations of total-, very low- and low density lipoprotein-cholesterol and elevated tri-acylglycerol levels. The HDL-cholesterol concentration was decreased, due to reduced concentrations of HDL2-subfractions. Significant changes in the composition of HDL2-subfractions were found in elderly untrained subjects. The HDL2-subfractions had more protein, a decreased apoA-I:A-II ratio and less phospholipids in comparison to HDL2-subfractions from younger untrained and trained, and elderly trained subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic low level physical activity as a determinant of high density lipoprotein cholesterol and subtractions

Physical activity has been associated with reduced risk of coronary heart disease. A mechanism for the reduced risk may be through increased high density lipoprotein cholesterol (HDL-C) and subfractions, in particular HDL2-C. Research associated with increased physical activity investigating HLD-C have assessed the effects of intense aerobic activity. The current research evaluated the relationship between low intensity, long duration activity to HDL-C and subfractions in 35 active postal carriers. Measurements of physical activity via the Large Scale Integrated monitor and reported miles walked, and lipoproteins were assessed at 3-month intervals over a 1-year period. Reported miles walked/day (5.3) was significantly correlated with HLD2-C (r = 0.50, P = 0.003) and approached significance for HDL-C (r = 0.29, P = 0.06). The Large Scale Integrated measures were correlated with HDL-C (r = 0.44, P = 0.008) and HDL2-C (r = 0.44, P = 0.007). Controlling for either age, alcohol consumption, body mass index, or leisure time activity did not reduce the relationship between reported miles walked or Large Scale Integrated readings and HDL2-C, suggesting that the increased HDL-C was the result of long duration, low intensity physical activity.

Effects of household sharing on high density lipoprotein and its subfractions.

Household effects accounted for significant proportions of the observed variance of high density lipoprotein cholesterol (HDL-C) and subfractions HDL2 and HDL3. It was found that 19.3% of HDL-C variance could be attributed to a juvenile sib effect (under age 18); 17.4% of HDL2 variance could be attributed to a sib effect (of any age); and 22.1% and 32.6% of the HDL3 variance could be attributed to a parent-offspring effect and a sib effect (of any age), respectively. In addition, additive genetic effects accounted for 56.5%, 37.3%, and 28.3% of the variances of HDL-C, HDL2, and HDL3, respectively. These are maximum likelihood estimates obtained using a variance components model on 2,149 HDL-C levels measured on members of 54 Utah pedigrees, and 337 HDL2 and HDL3 levels measured on a subset of 14 pedigrees.

Sedimentation equilibrium of human low density lipoprotein subfractions.

The molecular weights of low density lipoprotein (LDL) subfractions were determined precisely by meniscus depletion sedimentation equilibrium. Equilibrium speeds ranged from 9743 to 5896 rpm. The average molecular weights of various LDL subfractions of Sf values 9.49, 7.94, 6.42, 5.17, and 3.71 determined by sedimentation equilibrium were 2.97 X 10(6) ; 3.13 X 10(6); 2.89 X 10(6); 2.45 X 10(6); and 2.61 X 10(6) daltons, respectively; and their respective densities were 1.0267, 1.0306, 1.0358, 1.0422, and 1.0492 g/ml. Minimal hydrated molecular weights for this fractions determined by flotation velocity at 37,020 rpm were 2.57 X 10(6); 2.37 X 10(6); 2.09 X 10(6); 1.94 X 10(6); and 1.81 X 10(6) daltons; whereas similar molecular weights determined at 52,640 rpm were 2.53 X 10(6); 2.27 X 10(6); 1.99 X 10(6); 1.86 X 10(6); and 1.74 X 10(6) daltons for the respective LDL subfractions. Higher molecular weights of fractions 2 and 5 compared to their adjacent fractions 1 and 4 by sedimentation equilibrium are of great interest. The calculated fractional ratio f/f O from sedimentation equilibrium and flotation velocity data ranges from 1.10 to 1.31, suggesting complexity and asymmetry of LDL subfraction molecules. There is also evidence that compressibility of LDL molecules may be different than that for the salt solution under high g-force. Assuming that redistributed LDL molecules at equilibrium under low g-force are spherical, it is possible that the shape of LDL molecules undergoing flotation velocity determinations may be distorted in high g-force conditions. Such distortion may be consistent with the high f/f O values obtained and may also be a basis for structural rearrangement and/or lipoprotein degradation with prolonged preparative ultracentrifugation at high g-force and pressure.

The composition of low (LDL) and very low (VLDL) density lipoprotein subfractions in type III hyperlipoproteinaemia: Comparison with normal subjects

The lipid and protein composition of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) subfractions (Sf > 100, 60–100 and 20–60 VLDL and Sf 10.4–20, 5.7–12 and 3.5–6.5 LDL) in six subjects with type III hyperlipoproteinaemia (HLP) was compared to that of 12 normal subjects. In type III HLP all VLDL subfractions contained increased concentrations of cholesterol and triglyccrides and were relatively enriched in cholesterol.VLDL of Sf 20–60 also contained an increased concentration of B-protein. The tetramethylurea (TMU) soluble apolipoproteins of the VLDL subfractions were separated by polyacrylamide disc gel electrophoresis. In the subjects with type III HLP the proportion of arginine rich protein (ARP) was increased in all subfractions. The concentrations of cholesterol and triglycerides were increased in the LDL subfraction of Sf 10.4–20 and cholesterol was decreased in LDL of Sf 5.7–12, but the ratios of cholesterol to triglycerides were not significantly different from those in the LDL subfractions of the normal subjects and the protein composition was also similar. These results provide further evidence that in type III HLP abnormalities are not confined to the stage of conversion of VLDL to LDL, but occur throughout the VLDL spectrum.