Effects of dietary polyunsaturated and saturated fats on lipoproteins in the baboon

The effects of 2 different dietary fats (40% of calories from corn oil or coconut oil), in the presence of high-dietary cholesterol (1.7 mg/kcal), on the lipoprotein profiles of baboons (Papio cynocephalus sp) were studied by analytic ultracentrifugation, gradient gel electrophoresis (GGE), and heparin-manganese chloride precipitation. Relative to the corn oil (polyunsaturated fat) diet, the coconut oil (saturated fat) diet significantly increased total serum cholesterol by 43% (P less than 0.001) by increasing non-precipitable cholesterol (HDL-C) 58% (P less than 0.001) and precipitable cholesterol (VLDL + LDL-C) 35% (P less than 0.001). Analytic ultracentrifugal observations indicated that the increase in HDL-C was due to considerable increases in both HDL-I (baboon HDL of size 100-125 A and hydrated density 1.063-1.120 g/ml) and F1.20 degrees 9-28 lipoproteins (material of size 125-220 A and hydrated density 1.03-1.08 g/ml, and containing HDL apolipoproteins and apo E). Concentrations of other HDL subpopulations were unaffected by the dietary saturated rat. The increase in VLDL + LDL-C was due to increased LDL (S degree F 5-12 lipoproteins) and, to some extent, F1.20 degrees 9-28 lipoproteins because the larger, faster floating subspecies of the F1.20 degrees 9-28 lipoproteins were precipitable by heparin-manganese. In contrast, saturated fat (relative to polyunsaturated fat) induced lower concentrations of IDL (SF degree 12-20) and VLDL (SF degree 20-100). Lipoprotein size distributions by GGE indicated 5 HDL subpopulations and 2 or more LDL subpopulations in the sera of most baboons. The type of dietary fat did not affect the particle size range of each of the the HDL or LDL subpopulations. The results indicate that dietary fat markedly modulates the distribution of cholesterol between apo A-I-containing (HDL and F1.20 degrees 9-28) and apo B-containing (IDL and VLDL) lipoproteins without altering the presence of subpopulations based on particle size.     

A familial hyperalphalipoproteinemia with low uptake of high density lipoproteins into peripheral lymphocytes

A patient with an extremely high level of high density lipoprotein (HDL)-cholesterol and HDLc-like particles in the serum is discussed. The patient was a 46-year-old female with a serum total cholesterol concentration of 382 mg/dl and HDL-cholesterol level of 214 mg/dl. The HDL-cholesterol levels of her mother, brother, sister and 2 of her daughters were 82 mg/dl, 82 mg/dl, 74 mg/dl, 82 mg/dl and 82 mg/dl, respectively (mean HDL-cholesterol levels of control subjects: 52 +/- 6 mg/dl in males and 55 +/- 8 mg/dl in females). Her serum apolipoprotein A-I and E levels were elevated. Zonal ultracentrifugal analysis of her serum lipoproteins showed that the increased level of HDL-cholesterol was mainly due to HDL2; HDLc-like particles were also recognized between the LDL and HDL fractions. The incorporation of the patient's HDL and HDLc-like particles into cultured HepG2 cells was almost the same as that of HDL (1.063 less than d less than 1.21) from normal control serum. The incorporation of normal control HDL into the patient's peripheral blood lymphocytes was markedly less than that into lymphocytes from normal controls. These findings are discussed in terms of the reason for hyperalphalipoproteinemia in this patient.     

Gemfibrozil reduces small low-density lipoprotein more in normolipemic subjects classified as low-density lipoprotein pattern B compared with pattern A

We tested the hypothesis that gemfibrozil has a differential effect on low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subclass distributions and postprandial lipemia that is different in subjects classified as having LDL subclass pattern A or LDL pattern B who do not have a classic lipid disorder. Forty-three normolipemic subjects were randomized to gemfibrozil (1,200 mg/day) or placebo for 12 weeks. Lipids and lipoproteins were determined by enzymatic methods. The mass concentrations of lipoproteins in plasma were determined by analytic ultracentrifugation and included the S(f) intervals: 20 to 400 (very LDL), 12 to 20 (intermediate-density lipoprotein), 0 to 12 (LDL), and HDL(2) mass (F(1.20) 3.5 to 9.0) and HDL(3) mass (F(1.20) 0 to 3.5). Postprandial measurements of triglycerides and lipoprotein(a) were taken after the patients consumed a 500 kcal/M(2) test meal. Treatment with gemfibrozil, compared with placebo, significantly reduced fasting plasma triglycerides (difference from placebo +/- SE; -50.2 +/- 20.6 mg/dl, p = 0.02), total cholesterol (-16.4 +/- 7.5 mg/dl, p = 0.04), apolipoprotein B (-16.1 +/- 5.5 mg/dl, p = 0.006), very LDL mass of S(f) 20 to 400 (-50.8 +/- 24.1 mg/dl, p = 0.02), S(f) 20 to 60 (-17.5 +/- 8.5 mg/dl, p = 0.05), S(f) 60 to 100 (-16.2 +/- 8.1 mg/dl, p = 0.05), and increased peak S(F) (0.48 +/- 0.27 Svedberg, p = 0.08). Gemfibrozil reduced the postprandial triglyceride level significantly at 3 (p = 0.04) and 4 (p = 0.05) hours after the test meal. A significantly different subclass response to gemfibrozil was observed in those with LDL pattern A versus B. Those with LDL pattern B had a significantly greater reduction in the small LDL mass S(f) 0 to 7 (p = 0.04), specifically regions S(f) 0 to 3 (p = 0.009) and S(f) 3 to 5 (p = 0.009). In conclusion, normolipemic subjects with either predominantly dense or buoyant LDL respond differently to gemfibrozil as determined by the changes in LDL subclass distribution. Thus, treatment with gemfibrozil may have additional antiatherogenic effects in those with LDL pattern B by decreasing small dense LDL that is not apparent in those with pattern A.     

Effect of alcohol intake and exercise on plasma high-density lipoprotein cholesterol subfractions and apolipoprotein A-I in women

Abstinence from alcohol consumption for 3 weeks was followed by 3 weeks of wine intake in 18 inactive and 18 physically active premenopausal women (runners). The runners weighed less and had higher plasma high-density lipoprotein (HDL) cholesterol and lower low-density lipoprotein cholesterol levels than the inactive women. There were no differences between groups in plasma total cholesterol, triglyceride and apolipoprotein A-I concentrations. Runners had higher plasma HDL2 cholesterol concentrations than inactive women (34 +/- 17 vs 19 +/- 12 mg/dl), but HDL3 cholesterol concentration did not differ between the groups (41 +/- 10 vs 39 +/- 9 mg/dl). Addition of 35 g/day of ethanol for 3 weeks did not result in a significant change in either group for any of the variables measured. The amount of exercise appears to be a more important determinant of plasma lipoproteins and apolipoprotein A-I than alcohol intake in premenopausal women.     

Clinical evaluation of plasma high-density lipoprotein subfractions (HDL2, HDL3) in non-insulin-dependent diabetics with coronary artery disease

STATEMENT OF THE PROBLEM: Low levels of high-density lipoprotein cholesterol (HDL-C) have a strong association with coronary artery disease (CAD) in patients with non-insulin-dependent diabetes mellitus (NIDDM). In this study, we tried to evaluate whether one or both of the major HDL subclasses (HDL2, HDL3) is strongly associated with the risk of CAD in NIDDM subjects. METHODS: The separation of HDL subclasses was carried out by ultracentrifugation in a Beckman Airfuge. HDL2 subclass was isolated from the supernatant and its cholesterol content was measured enzymatically. Plasma HDL3 cholesterol was calculated as the difference between results for total HDL cholesterol and HDL2 cholesterol. RESULTS: NIDDM patients with CAD had significantly higher triglyceride levels compared to either control (217.09+/-55.04 versus 89.62+/-31.29 mg/dl, P=.001) or CAD patients without NIDDM (217.09+/-55.04 versus 156.28+/-46.39 mg/dl, P<.05). However, in the diabetic patients with CAD, there was a statistically significant decrease in HDL cholesterol (39.63+/-8.59 versus 55.86+/-13.49 mg/dl, P<.01), HDL2 cholesterol (8.74+/-3.28 versus 16.95+/-5.73 mg/dl, P<.001), and HDL3 cholesterol (31.23+/-7.41 versus 38.91+/-8.93 mg/dl, P<.05) in comparison to nondiabetic controls. Moreover, in the comparison between non-insulin-dependent diabetics with CAD and CAD subjects without NIDDM, HDL cholesterol (39.63+/-8.59 versus 46.13+/-6.33 mg/dl, P<.05) and HDL2 cholesterol (8.74+/-3.28 versus 11.84+/-4.01 mg/dl, P<.02) were significantly reduced, while HDL3 cholesterol levels were (31.23+/-7.41 versus 34.29+/-7.94 mg/dl, P=.92) unaltered. Additionally, the percentage reduction of cholesterol in HDL2 fraction was proportionately greater than the decrease in HDL3 subclass in both comparisons. Moreover, in NIDDM with CAD, HDL cholesterol was reduced by 29% and 14%, HDL2 cholesterol by 48% and 26%, and HDL3 cholesterol by 20% and 9%, compared relatively to controls and CAD subjects without NIDDM. CONCLUSIONS: In conclusion, HDL2 is the more variable subclass and reflects changes in HDL. This suggests that the protective role of total HDL against CAD is mainly mediated through HDL2 fraction. Therefore, HDL2 might be a better predictor of coronary heart disease than total HDL, in non-insulin-dependent diabetes mellitus.     

Influence of probucol administration on lipoprotein cholesterol and apolipoproteins in normolipemic males

In order to interpret the known lipoprotein changes in probucol-treated patients, serum concentrations of apolipoproteins (A-I, A-II, B, C-II, C-III, E) were measured before, during and after probucol administration (2 X 500 mg p.d.), in 16 healthy males (30.3 +/- 5.6 years old). Cholesterol concentrations were determined in LDL and VLDL fractions as well as in HDL subfractions which were isolated by preparative ultracentrifugation. In addition, apolipoprotein A-I and A-II concentrations were measured in the HDL subfractions. Compared with the baseline values, significant apolipoprotein changes were found in the serum apolipoprotein A-I (151 +/- 18 to 115 +/- 31 mg/dl; P less than 0.001) and C-II levels during administration. The HDL subfraction analysis showed that the decrease of HDL-cholesterol and apolipoprotein A-I (59.9 +/- 23.5 to 34.4 +/- 16.4 mg/dl, P less than 0.001, and 65.7 +/- 49.0 to 37.5 +/- 23.5 mg/dl, P less than 0.05, respectively) was predominantly related to the HDL2b subfraction (d = 1.063-1.100 g/ml).     

Lipoprotein(a) and apolipoprotein changes after cardiac transplantation

Although lipoprotein changes after cardiac transplantation have been documented, the effects of transplantation and subsequent immunosuppressive therapy (particularly the combination of prednisone, azathioprine and cyclosporine) on apolipoprotein levels and lipoprotein(a) have not been reported. Fasting cholesterol, triglycerides, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, apolipoprotein A-1 and B-100 and lipoprotein(a) were evaluated in 69 consecutive patients during the waiting period before cardiac transplantation. There were 28 deaths before donor organ identification and 41 patients received a cardiac allograft. The lipoprotein levels of transplant recipients were again assayed 3 months postoperatively. Mean (+/- SEM) values increased for total plasma cholesterol (from 180 +/- 8 to 228 +/- 8 mg/dl, p less than or equal to 0.001), triglycerides (from 126 +/- 11 to 207 +/- 14 mg/dl; p less than or equal to 0.001), HDL cholesterol (from 39 +/- 2 to 49 +/- 3 mg/dl; p less than or equal to 0.002) and LDL cholesterol (from 119 +/- 7 to 138 +/- 7 mg/dl; p less than 0.02). Apolipoprotein A-1 and B-100 also increased, but lipoprotein(a) decreased from 11.7 +/- 1.7 to 6.8 +/- 1.1 mg/dl; p less than or equal to 0.0001) after transplantation. Although total cholesterol, triglycerides, LDL cholesterol, apolipoprotein A-1 and B-100 increased dramatically after cardiac transplantation, so did HDL cholesterol, thereby keeping the LDL/HDL cholesterol ratio constant. The surprising decrease in lipoprotein(a) after cardiac transplantation suggests that metabolism of lipoprotein(a) is independent of LDL cholesterol and that immunosuppressive drugs either decrease the synthesis or increase catabolism of lipoprotein(a).     

High density lipoprotein metabolism in endurance athletes and sedentary men

BACKGROUND. Endurance athletes have higher high density lipoprotein (HDL) concentrations than sedentary controls. To examine the mechanism for this effect, we compared HDL apoprotein metabolism in 10 endurance athletes aged 34 +/- 6 years (mean +/- SD) and 10 sedentary men aged 36 +/- 8 years. METHODS AND RESULTS. Subjects were maintained on controlled diets for 4 weeks, and metabolic studies using autologously labeled 125I HDL were performed during the final 2 weeks. Lipids and lipoproteins were measured daily during these 2 weeks, and the average of 14 values was used in the analysis. HDL cholesterol (58 +/- 14 versus 41 +/- 10 mg/dl), HDL2 cholesterol (26 +/- 10 versus 12 +/- 8 mg/dl), and apolipoprotein A-I (apo A-I) (144 +/- 18 versus 115 +/- 22 mg/dl) were higher in the athletes, whereas triglyceride concentrations (60 +/- 18 versus 110 +/- 48 mg/dl) were lower (p less than 0.01 for all). Postheparin lipoprotein lipase activity was not different, but hepatic triglyceride lipase activity was 27% lower (p less than 0.06) in the athletes. The athletes' mean clearance rate of triglycerides after an infusion of Travamulsion (1 ml/kg) was nearly twofold that of the inactive men (5.8 +/- 1.5 versus 3.2 +/- 0.9%/min, p less than 0.001). There was no differences in HDL apoprotein synthetic rates, whereas the catabolic rates of both apo A-I (0.15 +/- 0.02 versus 0.22 +/- 0.05 pools per day, p less than 0.01) and apolipoprotein A-II (apo A-II) (0.15 +/- 0.02 versus 0.20 +/- 0.04 pools per day, p less than 0.05) were reduced in the trained men. Apo A-I and apo A-II half-lives correlated with HDL cholesterol in each group (r greater than 0.76, p less than 0.05 for all) but not consistently with lipase activities or fat clearance rates. This relation between apoprotein catabolism and HDL cholesterol was strongest at HDL cholesterol concentrations of less than 60 mg/dl. CONCLUSIONS. We conclude that higher HDL levels in active men are associated with increased HDL protein survival. The mechanisms mediating this effect require better definition, and other factors appear to contribute to HDL cholesterol and protein concentrations among individual subjects.     

Serum HDL cholesterol values are associated with apoB-containing lipoprotein metabolism and triglyceride-body fat interrelation in young Japanese men

Serum levels of total cholesterol, high density lipoprotein (HDL) cholesterol, triglyceride, apolipoprotein (apo) AI, ApoB, ApoE and body fat were measured in 226 fasting male Japanese college students aged 18 to 20 years. They were normolipidemic (total cholesterol: 169±31 mg/dl, triglyceride: 56±25 mg/dl) and their HDL cholesterol concentrations were high (61±13 mg/dl). An HDL cholesterol value <35 mg/dl was observed in only one student (0.4%). In contrast, 112 men (49.6%) had an HDL cholesterol level ≥60 mg/dl. Even in this normolipidemic group, as compared with students in a top HDL cholesterol tertile (HDL cholesterol; 75±9 mg/dl), students in a lower HDL cholesterol tertile (HDL cholesterol; 48±5 mg/dl) had significantly increased serum levels of LDL cholesterol (103±30 vs. 91±26 mg/dl), triglyceride (68±30 vs. 45±16 mg/dl) and apoB (83±20 vs 73±17 mg/dl). In addition, they had greater body mass index (23.2±3.6 vs. 20.6±2.5 kg/m²) and greater percent body fat (20.2±6.2 vs. 16.2±4.2%) determined using a bioelectrical impedance analyzer. HDL cholesterol levels were much more strongly related to triglyceride (r=−0.37) than was apoAI (r=−0.13). In stepwise multiple regression analysis in 184 nonsmokers, apoE, apoB and fat mass explained 21% of apoAI variability. Triglyceride in addition to these three parameters explained 41% of HDL cholesterol variability. These results suggest that serum levels of HDL cholesterol are associated with metabolism of apoB-containing lipoproteins as well as triglyceride-body fat interrelationship.     

Susceptibility of apolipoprotein B-containing lipoproteins to oxidation and antioxidant status in acute coronary syndromes

BACKGROUND: Oxidized lipoproteins may play an important role in the pathogenesis of atherosclerosis, and it has been shown that antioxidants have a protective effect against the progression of atherosclerosis. HYPOTHESIS: The aim of this study was to investigate the oxidative susceptibility of apolipoprotein B-containing lipoproteins and antioxidant status in patients with acute coronary syndromes and chronic stable angina pectoris. METHODS: The study population included 70 patients with acute coronary syndromes (14 with recent acute myocardial infarction and 56 with unstable angina pectoris), 105 patients with stable angina pectoris, and 75 control subjects. In addition to conventional lipid and lipoprotein analysis, the susceptibility of apolipoprotein B-containing lipoproteins to in vitro oxidation (lag phase) and plasma vitamin E and total carotene levels was measured. RESULTS: The lag phase was significantly shorter in patients with acute coronary syndromes (45 +/- 12 min) than in patients with stable angina pectoris (51 +/- 10 min) and in control subjects (58 +/- 9 min) (p < 0.0001). Both plasma vitamin E and total carotene levels were lowest in patients with acute coronary syndromes (1.11 +/- 0.32 mg/dl and 119 +/- 32 micrograms/dl, respectively), followed by patients with stable angina pectoris (1.25 +/- 0.37 mg/dl and 132 +/- 37 micrograms/dl) and then controls (1.52 +/- 0.31 mg/dl and 167 +/- 41 micrograms/dl). CONCLUSIONS: These data suggest that there is an intense oxidative process and a lower antioxidant status in acute coronary syndromes. This may lead to plaque instability due to the activation of the inflammatory response in coronary atherosclerotic lesions.     

Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease.

The prevalence of abnormalities of lipoprotein cholesterol and apolipoproteins A-I and B and lipoprotein (a) [Lp(a)] was determined in 321 men (mean age 50 +/- 7 years) with angiographically documented coronary artery disease and compared with that in 901 control subjects from the Framingham Offspring Study (mean age 49 +/- 6 years) who were clinically free of coronary artery disease. After correction for sampling in hospital, beta-adrenergic medication use and effects of diet, patients had significantly higher cholesterol levels (224 +/- 53 vs. 214 +/- 36 mg/dl), triglycerides (189 +/- 95 vs. 141 +/- 104 mg/dl), low density lipoprotein (LDL) cholesterol (156 +/- 51 vs. 138 +/- 33 mg/dl), apolipoprotein B (131 +/- 37 vs. 108 +/- 33 mg/dl) and Lp(a) levels (19.9 +/- 19 vs. 14.9 +/- 17.5 mg/dl). They also had significantly lower high density lipoprotein (HDL) cholesterol (36 +/- 11 vs. 45 +/- 12 mg/dl) and apolipoprotein A-I levels (114 +/- 26 vs. 136 +/- 32 mg/dl) (all p less than 0.005). On the basis of Lipid Research Clinic 90th percentile values for triglycerides and LDL cholesterol and 10th percentile values for HDL cholesterol, the most frequent dyslipidemias were low HDL cholesterol alone (19.3% vs. 4.4%), elevated LDL cholesterol (12.1% vs. 9%), hypertriglyceridemia with low HDL cholesterol (9.7% vs. 4.2%), hypertriglyceridemia and elevated LDL cholesterol with low HDL cholesterol (3.4% vs. 0.2%) and Lp(a) excess (15.8% vs. 10%) in patients versus control subjects, respectively (p less than 0.05). Stepwise discriminant analysis indicates that smoking, hypertension, decreased apolipoprotein A-I, increased apolipoprotein B, increased Lp(a) and diabetes are all significant (p less than 0.05) factors in descending order of importance in distinguishing patients with coronary artery disease from normal control subjects. Not applying a correction for beta-adrenergic blocking agents, sampling bias and diet effects leads to a serious underestimation of the prevalence of LDL abnormalities and an overestimation of HDL abnormalities in patients with coronary artery disease. However, 35% of patients had a total cholesterol level less than 200 mg/dl after correction; of those patients, 73% had an HDL cholesterol level less than 35 mg/dl.     

Plasma HDL levels highly correlate with cognitive function in exceptional longevity

BACKGROUND: Families of centenarians have high levels of plasma high-density lipoprotein (HDL) cholesterol, which may have neurological as well as cardiovascular protective effects during aging. Because plasma HDL level declines progressively with aging, we examined whether centenarians with higher plasma HDL levels have better cognitive function. METHODS: Total plasma cholesterol, low-density lipoprotein (LDL) cholesterol, HDL, triglycerides, and apolipoprotein levels were measured in a group of centenarians (N = 139; older than 95 years) and were correlated with their cognitive function (measured by Mini-Mental State Examination [MMSE]). RESULTS: Plasma HDL levels correlated significantly with MMSE (r =.32; p <.0001). Each decrease in plasma HDL tertile (74.9 +/- 2.1, 50.6 +/- 0.5, and 36.8 +/- 1.0 mg/dl) was associated with a significant decrease in MMSE (23.4 +/- 1.5, 17.7 +/- 1.8, and 12.4 +/- 1.8; p <.04 for each plasma HDL tertile). As expected, increased plasma apolipoprotein A-I and decreased plasma triglyceride levels were also correlated with a significantly superior cognitive function. Biological markers of hydration and nutritional status did not differ between the groups with the higher or lower plasma HDL or MMSE. CONCLUSIONS: These data demonstrate that cognitive dysfunction in centenarians is associated with a progressive decline in plasma HDL concentrations. This underscores the protective effects of increased plasma HDL and its role in maintaining superior cognition in longevity.     

Distribution of ApoA-I-containing HDL subpopulations in patients with coronary heart disease

High density lipoproteins (HDLs) and their subspecies play a role in the development of coronary heart disease (CHD). HDL subpopulations were measured by 2-dimensional nondenaturing gel electrophoresis in 79 male control subjects and 76 male CHD patients to test the hypothesis that greater differences in apolipoprotein (apo)A-I-containing HDL subpopulations would exist between these 2 groups than for traditional lipid levels. In CHD subjects, HDL cholesterol (HDL-C) was lower (-14%, P<0.001), whereas total cholesterol and the low density lipoprotein cholesterol/HDL-C ratio were higher (9% [P:<0.05] and 21% [P:<0.01], respectively) compared with control levels. No significant differences were found for low density lipoprotein cholesterol, triglyceride, and apoA-I levels. In CHD subjects, there were significantly (P:<0.001) lower concentrations of the large lipoprotein (Lp)A-I alpha(1) (-35%), pre-alpha(1) (-50%), pre-alpha(2) (-33%), and pre-alpha(3) (-31%) subpopulations, whereas the concentrations of the small LpA-I/A-II alpha(3) particles were significantly (P:<0.001) higher (20%). Because alpha(1) was decreased more than HDL-C and plasma apoA-I concentrations in CHD subjects, the ratios of HDL-C to alpha(1) and of apoA-I to alpha(1) were significantly (P:<0.001) higher by 36% and 57%, respectively, compared with control values. Subjects with low HDL-C levels (35 mg/dL). Therefore, we stratified participants according to HDL-C concentrations into low and normal groups. The differences in lipid levels between controls and HDL-C-matched cases substantially decreased; however, the significant differences in HDL subspecies remained. Our research findings support the concept that compared with control subjects, CHD patients not only have HDL deficiency but also have a major rearrangement in the HDL subpopulations with significantly lower alpha(1) and pre-alpha(1-3) (LpA-I) and significantly higher alpha(3) (LpA-I/A-II) particles.     

Aerobic exercise, lipids and lipoproteins in overweight and obese adults: a meta-analysis of randomized controlled trials

OBJECTIVE: Use the meta-analytic approach to examine the effects of aerobic exercise on lipids and lipoproteins in overweight and obese adults. DATA SOURCES: (1) Computerized literature searches, (2) cross-referencing from review and original articles, (3) hand searching, and (4) expert review of reference list. STUDY SELECTION: (1) randomized controlled trials, (2) aerobic exercise > or =8 weeks, (3) adult humans > or =18 y of age, (4) all subjects overweight or obese (BMI > or =25 kg/m(2)), (5) studies published in journal, dissertation, or master's thesis format, (6) studies published in the English-language, (7) studies published between 1 January 1955 and 1 January 2003, (8) assessment of one or more of the following lipid and/or lipoprotein variables: total cholesterol (TC), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), and triglycerides (TG). DATA ABSTRACTION: Dual-coding by the first two authors (inter-rater agreement=0.96). RESULTS: In total, 13 studies representing 31 groups (17 exercise, 14 control), 613 subjects (348 exercise, 265 control), and up to 17 outcomes were available for pooling. Across all categories, random-effects modeling resulted in statistically significant improvements for TC (X +/- s.e.m., - 3.4+/-1.7 mg/dl, 95% CI, - 6.7 to - 0.2 mg/dl) and TG (X +/-s.e.m., - 16.1+/-7.3 mg/dl, 95% CI, - 30.2 to - 2.1 mg/dl) but not HDL (X +/- s.e.m., 1.6+/-0.8 mg/dl, 95% CI, - 0.02 to 3.2 mg/dl) or LDL (X +/-s.e.m., - 0.5+/-1.3 mg/dl, 95% CI, - 3.0 to 2.0 mg/dl). Changes were equivalent to improvements of 2% (TC), 11% (TG), 3% (HDL), and 0.3% (LDL). After conducting sensitivity analyses (each study deleted from the model once), only decreases in TG remained statistically significant. Increases in HDL were associated with increases in maximum oxygen consumption (VO(2 max) in ml/kg/min, r=0.75, P=0.002) and decreases in body weight (r=0.77, P<0.001), while decreases in LDL were associated with decreases in body weight (r=0.75, P=0.009). CONCLUSIONS: Aerobic exercise decreases TG in overweight and obese adults. However, a need exists for additional randomized controlled trials in various overweight and/or obese populations above and beyond those included in our analysis.     

Exercise, diet, or physical characteristics as determinants of HDL-levels in endurance athletes

Serum lipids, lipoproteins, apolipoproteins, physical characteristics, and 10-day dietary records of 20 male distance runners (aged 20-42 years) were compared with those of 14 sedentary controls (aged 23-34 years). Runners had significantly greater levels (mean +/- SD) of high density lipoproteins (HDL) whether estimated as HDL-cholesterol (66 +/- 12 vs 46 +/- 10 mg/dl) or as the major HDL apolipoproteins, apoA-I (170 +/- 36 vs 124 +/- 27 mg/dl) or apoA-II (39 +/- 5 vs 34 +/- 4 mg/dl). Runners were leaner with considerably less body fat (8.3 +/- 1.7 vs 16.2 +/- 3.9%) than the sedentary men despite consuming 20% more calories. Moreover, the additional calories consumed were largely carbohydrate. This comparison illustrates that high absolute quantities of dietary carbohydrate do not depress HDL levels in lean individuals engaged in exercise training. Furthermore, the results suggest that dietary factors may be as important as exercise itself in producing the lipoprotein pattern characteristic of endurance athletes.     

Apolipoprotein E genotype and exercise training-induced increases in plasma high-density lipoprotein (HDL)- and HDL2-cholesterol levels in overweight men.

We determined if the apolipoprotein E (APO E) genotype affects the exercise training-induced increase in plasma high-density lipoprotein cholesterol (HDL-C) and HDL2-C. Sedentary overweight men on an American Heart Association (AHA) step I diet had plasma lipoprotein-lipids measured before and after 9 months of endurance exercise training. APO E2 (n = 6), E3 (n = 33), and E4 (n = 12) groups were similar at baseline in terms of age, body weight and composition, and plasma lipoprotein-lipid profiles. APO E2 men had a larger increase in plasma HDL-C and HDL2-C with exercise training than APO E3 and E4 men (HDL-C, 8 +/- 4 v 3 +/- 1 v 2 +/- 1 mg/dL; HDL2-C, 5 +/- 3 v 1 +/- 1 v -1 +/- 1 mg/dL; mean +/- SE, all P < .01). After adjusting for body weight changes, the increases in plasma HDL-C and HDL2-C remained greater in APO E2 versus E3 and E4 men (all P < .03). These results indicate that APO E2 men may have greater plasma HDL-C and HDL2-C increases with endurance exercise training.     

Expression of the human apolipoprotein A-I gene in transgenic mice alters high density lipoprotein (HDL) particle size distribution and diminishes selective uptake of HDL cholesteryl esters.

Transgenic mice carrying the human apolipoprotein (apo) A-I gene (HuAITg mice) were used to examine the effects of overexpression of the human gene on high density lipoprotein (HDL) particle size distribution and metabolism. On a chow diet, control mice had HDL cholesterol and apo A-I levels of 49 +/- 2 and 137 +/- 12 mg/dl of plasma, respectively. HuAITg mice had HDL cholesterol, human apo A-I, and mouse apo A-I levels of 88 +/- 2, 255 +/- 19, and 16 +/- 2 mg/dl, respectively. Nondenaturing gradient gel electrophoresis revealed control mouse plasma HDL to be primarily monodisperse with a particle diameter of 10.2 nm, whereas HuAITg mouse plasma HDL was polydisperse with particles of diameter 11.4, 10.2, and 8.7 nm, which correspond in size to human HDL1, HDL2, and HDL3, respectively. In vivo turnover studies of HDL labeled with [3H]cholesteryl linoleyl ether (representing the cholesteryl ester pool) and 125I-apo A-I were performed. In control animals, the fractional catabolic rate (FCR) for HDL cholesteryl ester (0.197 +/- 0.010 pool/hr) was significantly (P less than 0.0005) more than the apo A-I FCR (0.118 +/- 0.006 pool/hr). In the HuAITg mice, the HDL cholesteryl ester FCR (0.124 +/- 0.008 pool/hr) was the same as the apo A-I FCR (0.126 +/- 0.010 pool/hr). There were no significant differences between control and HuAITg animals in the sites of tissue removal of HDL cholesteryl ester, with the liver extracting most of the injected radioactivity. Control and HuAITg animals had comparable liver and intestinal cholesterol synthesis and LDL FCR. In conclusion, HuAITg mice have principally human and not mouse apo A-I in their plasma. This apparently causes a change in HDL particle size distribution in the transgenic mice to one resembling the human pattern. The replacement of mouse by human apo A-I also apparently causes the loss of the selective uptake pathway of HDL cholesteryl esters present in control mice. These data imply that apo A-I primary structure has a profound influence on HDL particle size distribution and metabolism.     

Influence of obesity and hypertriglyceridaemia on the low HDL2-cholesterol level and on its relationship with prevalence of atherosclerosis in type 2 diabetes.

High density lipoprotein subfraction 2 (HDL1)-cholesterol level is usually decreased in Type 2 (non-insulin-dependent) diabetes. A study was carried out in 251 Type 2 diabetic patients (106 males [M], 145 females [F]) and in 120 non diabetic controls in order to determine the influence of hypertriglyceridaemia and obesity on the HDL2-cholesterol level and to analyse the relationship between HDL2-cholesterol level and atherosclerosis (coronary heart disease, peripheral atherosclerosis or cerebral vascular disease), in Type 2 diabetes. Influence of hypertriglyceridaemia and obesity on HDL2-cholesterol level was studied by comparing the mean values of HDL2-cholesterol between diabetics and controls, after controlling for hypertriglyceridaemia and obesity, and by a multiple linear regression test. A stepwise logistic regression was performed to analyse the association between the prevalence of atherosclerosis and several variables: age, duration of diabetes, hypertension, cigarette smoking, body mass index, mean glycaemia, total cholesterol, triglyceride, HDL-cholesterol, HDL2-cholesterol and HDL3-cholesterol levels. In both men and women, when both of the factors (hypertriglyceridaemia and obesity) were present of when only one was, HDL2-cholesterol level was significantly lower in the diabetic population, compared with controls. But when obesity and hypertriglyceridaemia were absent, HDL2-cholesterol level, in the diabetic population, was not significantly different from controls (M: 17.9 +/- 13.3 vs 20.5 +/- 13.8 mg/dl: NS; F: 30.1 +/- 21.5 vs 27.6 +/- 14.2 mg/dl: NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

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/1 cholesterol, P less than 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 less than 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.     

Aerobic exercise and HDL2-C: a meta-analysis of randomized controlled trials

PURPOSE: Use the meta-analytic approach to examine the effects of aerobic exercise on high-density lipoprotein two cholesterol (HDL2-C) in adults. STUDY SOURCES: (1) Computerized literature searches; (2) cross-referencing from retrieved articles; (3) hand-searching; and (4) expert review of our reference list. STUDY SELECTION: (1) Randomized controlled trials; (2) aerobic exercise > or = 8 weeks; (3) adults > or = 18 years of age; (4) studies published in journal, dissertation, or master's thesis format; (5) studies published in the English-language between January 1, 1955 and January 1, 2003; and (6) assessment of HDL2-C in the fasting state. DATA ABSTRACTION: All coding conducted by both authors, independent of each other. Discrepancies were resolved by consensus. RESULTS: Nineteen randomized controlled trials representing 20 HDL2-C outcomes from 984 males and females (516 exercise, 468 control) were pooled for analysis. Using random-effects modeling and bootstrap confidence intervals (BCI), a statistically significant increase of approximately 11% was observed for HDL2-C (X +/- S.E.M., 2.6 +/- 0.9 mg/dl, 95% BCI, 1.0-4.4 mg/dl). With each study deleted from the model once, results remained statistically significant. Increases in HDL2-C were independent of decreases in body weight, body mass index (kg/m2), and percent body fat. CONCLUSION: Aerobic exercise increases HDL2-C in adults.