Total HDL Concentrations Research Articles

Effect of short term aerobic exercise on fasting and postprandial lipoprotein subfractions in healthy sedentary men.

BackgroundOur goal was to investigate the effect of short term exercise on fasting and postprandial lipoprotein profile.MethodsHealthy sedentary men exercised 20 min for four days. The intensity of exercise was modulated to maintain 75–80 % of a calculated HRmax. Before and after the exercise program, fasting and postprandial (4 h after standard meal) concentrations of lipoprotein subfractions were measured by an electrophoresis in polyacrylamide gel and total concentrations of TAG, LDL and HDL by enzymatic colorimetric method. After 2 days of rest, fasting and postprandial concentrations of lipoprotein fractions and subfractions were measured to determine a persistency of a changes in the lipoprotein profile.Results4 days of physical exercise led to statistically significant decrease of concentration of triacylglycerol in fasting (76.29 ± 20.07, 53.92 ± 10.90, p < 0.05) and postprandial state (139.06 ± 23.72, 96.55 ± 25.21, p < 0.05) VLDL in fasting (21.88 ± 3.87, 18.00 ± 3.93, p < 0.05) and postprandial state (23.88 ± 3.52, 19.25 ± 3.62, p < 0.05), total cholesterol in fasting (162.26 ± 23.38, 148.91 ± 17.72, p < 0.05) and postprandial state (163.73 ± 23.02, 150.08 ± 18.11, p < 0.05). Atherogenic medium LDL decreased also in fasting (9.89 ± 3.27, 6.22 ± 2.55, p < 0.001) and postprandial state (8.88 ± 6.51, 6.88 ± 5.57, p < 0.001). However decrease of large IDL (25.38 ± 3.54, 23.88 ± 3.91, p < 0.05) and large LDL particles (42.89 ± 11.40, 38.67 ± 9.30) was observed only in postprandial state. Total HDL concentration remained unchanged but we observed statistically significant decrease of small HDL particles in fasting (6.11 ± 2.89, 4.22, p < 0.05) and postprandial state (6.44 ± 3.21, 4.56 ± 1.33, p < 0.05). Concentration of these particles are associated with progression of atherosclerosis. All changes of fasting and postprandial lipoprotein profile disappeared after 2 days of rest.ConclusionJust 4 daily settings of 20 min of physical exercise can lead to significant positive changes of fasting and postprandial lipoprotein profile.

Abstract 37: Association between High-Density Lipoprotein Cholesterol Subfractions and Carotid Intima-Media Thickness

Background Recent trials have challenged the protective effect of HDL in atherosclerosis, implicating the need to shift the focus from total HDL concentration to its function and major subfractions. The objective of this cross-sectional study was to investigate the relation between HDL2 and HDL3 subfractions and carotid intima-media thickness (IMT), an early indicator of atherosclerosis and surrogate marker of ischemic stroke. Methods In NOMAS, a prospective population-based study of the incidence and risk factors of stroke, we evaluated 1041 participants (mean age 68±9 years; 38% men; 62% Hispanic, 19% black, 17% white) with available data on HDL subfractions and carotid IMT assessed by a high-resolution 2D carotid ultrasound. Carotid IMT was a composite measure of the mean IMT in all carotid artery segments. The cross-sectional association between HDL-subfractions and IMT was analyzed by multiple linear regression. Results We mean±SD of total HDL was 46.15±14.25 mg/dl (median = 44.00), HDL2 14.59±8.29 mg/dl (median = 13.00), HDL3 31.06±8.32 mg/dl (median = 32.00). The mean IMT was 0.90±0.08 mm. After controlling for demographics, LDL, triglycerides, and cholesterol-lowering medication, a strong association was observed between total HDL (per SD, beta=-0.008, p= 0.01), HDL2 (per SD, beta=-0.006, p=0.03) and HDL3 (per SD, beta=-0.007 p=0.01) in relation to IMT. A significant interaction was observed between diabetes (vs. non-diabetes) and HDL2 in relation to IMT (p=0.01; -0.018mm). Conclusion The observed strong independent inverse associations between HDL, HDL2 and HDL3 and carotid IMT. HDL2 was only significantly associated with IMT among individuals with diabetes. These observations show novel evidence for a potential role of HDL2 and HDL3 subfractions, providing the opportunity to develop novel HDL-targeted therapies for the prevention of atherosclerosis.

High-density lipoprotein subclasses are a potential intermediary between alcohol intake and reduced risk of cardiovascular disease: The Rancho Bernardo Study

We conducted a cross-sectional study of NMR-derived HDL subclasses and alcohol intake among 2171 community-dwelling older adults with a large proportion of daily or near-daily alcohol consumers (44 %). We aimed to assess whether, in addition to increasing total HDL, alcohol may induce a beneficial shift in HDL particle size distribution. Participants were categorised based on reported alcohol intake (g per week) and on frequency (none, < 3 times/week, 3-4 times/week, ≥ 5 times/week). The association between alcohol intake and lipoprotein fractions was examined using sex-specific linear regression models adjusted for age, BMI, diabetes, current smoking, exercise and hormone therapy in women. There was a stepwise gradient with the highest weekly alcohol consumption associated with the highest total HDL size and greatest number of medium and large HDL particles, as well as higher total HDL concentrations (all P < 0.001); total small HDL did not differ. Alcohol-HDL size associations were similar in both sexes and did not differ by use of hormone replacement therapy in women. In conclusion, regular alcohol consumers had a higher number and percentage of large HDL particles than non-drinkers. These results suggest that one way that alcohol may decrease CVD is through potentially favourable changes in lipoprotein subclass composition.

Effect of obesity on the plasma lipoprotein subclass profile in normoglycemic and normolipidemic men and women.

To determine the effect of obesity without the confounding effect of metabolic complications on the lipoprotein subclass profile in men and women. Cross-sectional study. A total of 40 lean (body mass index (BMI): 18.5-25 kg/m(2)) and 40 obese (BMI: 30-45 kg/m(2)) subjects, with blood pressure <140/90 mm Hg, fasting plasma glucose concentration <100 mg per 100 ml and total triglyceride concentration <150 mg per 100 ml; all obese subjects had normal oral glucose tolerance. Fasting concentrations of very low-, intermediate-, low- and high-density lipoproteins (VLDL, IDL, LDL, and HDL, respectively) and average VLDL, LDL and HDL particle sizes were evaluated by using proton nuclear magnetic resonance spectroscopy. Obese compared with lean individuals of both sexes had increased plasma concentrations of VLDL (by approximately 50%), IDL (by approximately 100%), LDL (by approximately 50%), and to some extent HDL (by approximately 10%) particles (P<0.05). The contribution of large VLDL to total VLDL concentration, small LDL to total LDL concentration, and small HDL to total HDL concentration was greater in obese than lean subjects (P<0.05), resulting in larger average VLDL size but smaller average LDL and HDL sizes (P<0.05). Women, compared with men, had reduced concentrations of total VLDL particles (by approximately 10%) due to lower concentrations of large and medium VLDL and a shift toward large at the expense of small HDL particles (P<0.05), with no difference in total HDL particle concentration. IDL and total LDL concentrations and LDL subclass distribution were not different between men and women. Obesity is associated with pro-atherogenic alterations in the lipoprotein subclass profile, which may increase cardiovascular disease risk even in the absence of classical metabolic risk factors. On the other hand, the female cardiovascular disease risk advantage is probably largely related to differences in traditional lipid risk factors (plasma triglyceride and HDL-cholesterol concentrations) because sex differences in the plasma lipoprotein subclass profile are minimal.

The Apolipoprotein E Phenotype Has a Strong Influence on Tracking of Serum Cholesterol and Lipoprotein Levels in Children: A Follow-Up Study from Birth to the Age of 11 Years

The extent to which an individual maintains his position relative to the rest of the population is called tracking. The objective of this study was to examine the effect of the apolipoprotein E (apoE) phenotype on the tracking of serum cholesterol and lipoproteins from birth to the age of 11 y. In a longitudinal follow-up study of healthy children, concentrations of total serum cholesterol and triglyceride were determined at birth (n = 193), and at the ages of 2 (n = 192), 4 (n = 192), 6 (n = 190), 9 (n = 188), and 12 mo (n = 196), and 5 (n = 162) and 11 y (n = 153). Concentrations of total HDL, HDL2, and HDL3, VLDL, and LDL cholesterol were determined at 2, 6, 9, and 12 mo (n = 36), and 5 (n = 162) and 11 y (n = 153). The apoE phenotype was determined in 151 children. The children had the following apoE phenotypes: 4 had type 4/4 and 40 type 3/4 (group apoE4), 94 had type 3/3 (group apoE3), and 11 had type 2/3 and 2 type 2/4 (group apoE2). The correlation coefficients for total cholesterol levels during childhood compared with the level at 11 y of age were: 0.03 at birth, 0.26 (p < 0.001) at 2 mo, 0.24 (p < 0.001) at 4 mo, 0.24 (p < 0.001) at 6 mo, 0.28 (p < 0.001) at 9 mo, 0.41 (p < 0.001) at 12 mo, and 0.60 (p < 0.001) at 5 y. When the children were divided into three groups according to their apoE phenotypes, these three groups had the following correlation coefficients at 4 mo, 12 mo, or 5 y of age compared with the level at the age of 11 y; group apoE2: r = 0.65 (p < 0.01), r = 0.59 (p < 0.01), and r = 0.72 (p < 0.01); group apoE3: r = 0.27 (p < 0.01), 0.43 (p < 0.001), and r = 0.64 (p < 0.001); and group apoE4: r = 0.14 (p = NS), r = 0.33 (p < 0.05), and 0.42 (p < 0.01). The apoE phenotype also strongly influenced the tracking of the LDL cholesterol levels; the correlation coefficients between 5 and 11 y of age were for group apoE2 r = 0.84 (p < 0.001), for group apoE3 r = 0.70 (p < 0.001), and for group apoE4 r = 0.37 (p < 0.05). Our results indicate that the apoE phenotype strongly influences the tracking of lipids. The children having apoE 2/3, 2/4, and 3/3 phenotypes maintained their relative cholesterol and lipoprotein levels better than the others throughout the first 11 y of age. Because the apoE phenotype strongly affects the tracking of serum cholesterol, the usefulness of cholesterol screening in predicting future cholesterol values should be analyzed, keeping the apoE phenotype in mind.

Anomalies in composition of uremic lipoproteins isolated by gradient ultracentrifugation: relative enrichment of HDL in apolipoprotein C-III at the expense of apolipoprotein A-I

Using a discriminating gradient separation technique combined with careful analysis of lipid and apolipoprotein (apo) composition, serum lipoproteins of 20 chronically uremic patients have been compared with those of 19 normal controls matched for age and sex. In uremic subjects, serum VLDL concentration was markedly increased. These particles were enriched in protein and cholesterol and relatively poor in triglycerides (TG). They contained more frequently apo B-48, and a decreased proportion of apo E. Expressed in percent, total apo C was normal but the ratio of apo C-III 2/apo C-III 1 was elevated. Uremic IDL, whose serum concentration was markedly increased, were characterized by an increased proportion of protein. Total uremic LDL whose serum concentration was normal, contained less esterified cholesterol (EC) and more TG than normal LDL, their EC TG ratio being very low. Moreover, the concentration of the mature subfraction of LDL having a mean density of 1.043 g/ml, was markedly decreased in uremic subjects. Taken together, these anomalies indicate a delayed transformation of VLDL into LDL in chronic renal failure. The decreased concentration of total HDL in uremic subjects was more marked in HDL 2 (−46%) than HDL 3 (−24%). Both uremic HDL 3 and HDL 3 were relatively enriched in TG, and uremic HDL 3 were poorer in EC than normal HDL 3. The most striking abnormality of uremic HDL was however the marked relative enrichment of these lipoprotein particles in apo C at the expense of apo A-I (HDL 2: 25.3 ± 7.7% vs. 12.5 ± 5.3% for apo C and 56.0 ± 11.2% vs. 71.1 ± 8.3% for apo A-I; HDL 3: 14.9 ± 10.6% vs. 5.9 ± 3.0% for apo C and 63.4 ± 11.1% vs. 72.9 ± 6.1% for apo A-I). Furthermore, the percent of apo C-II was significantly decreased in uremic HDL 2 and HDL 3 by comparison with normal HDL 2 and HDL 3 (15.9 ± 5.4% vs. 22.3 ± 6.7% and 17 7 ± 4.9% vs. 24.2 ± 5.8%, respectively) and that of apo C-III 2 was increased from 24 to 39.2% of total apo C in HDL 2 and from 20.8 to 36.3% in HDL 3. Such structural anomalies of HDL probably play an important role in the disturbed conversion of VLDL to LDL, and also in the interaction of HDL with peripheral tissues.

Characterization of HDL and lipoproteins intermediate to LDL and HDL in the serum of pedigreed baboons fed an atherogenic diet

A lipoprotein species with ultracentrifugal flotation rates ( F 1.20 0 9–28) intermediate to high density lipoproteins (HDL, F 1.20 0 0–9) and low density lipoproteins (LDL, F 1.20 0 28–56) found in the plasma of certain pedigreed baboons fed an atherogenic diet was studied by gradient gel electrophoresis (GGE) and ultracentrifugal techniques. These lipoproteins were found to be heterogeneous in size (125–220 Å) and hydrated density (1.028–1.080 g/ml). The major apolipoprotein in all density subfractions of the F .20 o 9–28 lipoproteins exhibited the molecular weight (2.8 × 10 4 daltons) and immunochemical properties of apolipoprotein A-1 (apoA-I). Protein corresponding to apolipoprotein E (apoE, 3.5 × 10 4 daltons),was observed primarily in the less dense subspecies of F 1.20 0 9–28 lipoproteins. Some low molecular weight (1.8 × 10 4, 1.3 × 10 4, and 1.1 × 10 4 daltons) apolipoproteins were also detected. At low serum F 1.20 0 9–28 lipoprotein concentrations, only the smaller, more dense, protein-rich species were present; at higher F 1.20 0 9–28 concentrations, the larger, less dense species were observed in addition to the small species. The HDL of pedigreed baboons in families with and without serum F 1.20 0 9–28 lipoproteins were also characterized. The HDL of both groups of progeny consisted of a similar set of 5 subpopulations designated HDL-I through HDL-V determined by GGE. HDL-I, consisting of material 100–125 Å in size, was the major HDL subpopulation. ApoA-I was the major protein moiety in all HDL subpopulations; none contained apoE. Baboons in families with F 1.20 0 9–28 lipoproteins had more HDL-I (292 ± 80 mg/dl vs. 235 ± 55 mg/dl) and less HDL-II (86 ± 22 mg/dl vs. 135 ± 34 mg/dl) than baboons in families without F 1.20 0 9–28 lipoproteins; both groups showed identical total HDL concentrations (446 ± 90 mg/dl and 444 ± 49 mg/dl, respectively). Among those baboons in families with F 1.20 0 9–28 lipoproteins, there was an inverse correlation between F 1.20 0 9–28 concentration and total HDL, HDL-I and HDL-II concentrations, indicating a possible metabolic relationship between these HDL subpopulations and the F 1.20 0 9–28 species.

Changes in HDL subfractions after a single, extended episode of physical exercise

In order to investigate the changes in HDL subfractions induced by a single period of extended physical exercise, 9 endurance-trained adults were examined before and 6 min, 1 and 6 h after a 30 km cross-country race. In contrast to less evident changes in the concentrations of total HDL, apolipoprotein A-I and A-II, there were significant changes in HDL subfractions. Resting levels of protein and cholesterol content of the HDL subfractions 1–3 increased (subfraction 1, density gradient 1.093: 1.68 ± 0.58 to 3.24 ± 0.86 mmol/l cholesterol, P < 0.001), while the concentrations in HDL subfractions 11–12 decreased proportionately (subfraction 12, density gradient 1.142: 3.68 ± 0.81 to 2.19 ± 0.22 mmol/1 cholesterol, P < 0.001). The results suggest that physical exercise induces an increased formation of HDL particles of lower density from HDL particles of higher density. It was concluded that this formation is related to the catabolism of triglyceride-rich lipoproteins in the post-exercise period.

Further evidence on the effect of vitamin E on the cholesterol distribution in lipoproteins with special reference to HDL subfractions.

Earlier claims that oral administration of alpha-tocopherol results in significant and considerable increase in the serum total HDL concentration could not be substantiated. The present investigation does, however, show that lipoproteins are affected by alpha-tocopherol in other ways, the main effects being an increase in LDL-cholesterol and also in the HDL3-V cholesterol, an HDL3-subfraction determined by polyacrylamide gel electrophoresis. The established lipoprotein risk indices (LDL/HDL and HDL3/HDL2 ratios) were unfavorably affected as a result of alpha-tocopherol treatment. It is concluded that on the basis of available evidence, there is no reason to believe that alpha-tocopherol has a role to play in the prevention and treatment of atherosclerotic disease.