Effects of acute exercise intensity on plasma lipids and apolipoproteins in trained runners.

The purpose of this study was to determine the effects of exercise intensity on lipid and lipoprotein metabolism. Concentrations of triglyceride, cholesterol, high-density lipoprotein cholesterol (HDL-C) and its subfractions (HDL2-C and HDL3-C), low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, and apolipoproteins A-I, A-II, and B were measured. Ten well-trained runners completed treadmill exercise on two different occasions: a high-intensity session at 75% maximal oxygen consumption lasting 60 min and a low-intensity session at 50% maximal oxygen consumption lasting 90 min. Energy expenditure for each session was equal. Fasted blood samples were obtained 24 h before, immediately before, immediately after, and 1, 24, 48, and 72 h after each exercise session. No significant differences were found for the blood variables across time or between treatments. However, HDL-C and HDL2-C were slightly elevated on the days after each treatment. These results suggest that acute exercise sessions lasting less than 90 min, regardless of intensity, do not elicit plasma lipid, lipoprotein, and apolipoprotein changes in men who are habitually physically active and have high initial concentrations of HDL-C.     

Paraoxonase activity and concentration of indicators of lipids status in the serum of cardiac patients

In this research, we measured the activity of paraoxonase (basal and activated) enzyme, and components of lipid status components (total cholesterol, LDL cholesterol, HDL cholesterol and Apo A I) in the serum of patients, undergoing bypass surgery. We also tested how the applied EKC affected changes of defined indicators. Measuring of all the given parameters was conducted prior to the operation, 90 minutes, 1.5 hour, 6 hours, 24 hours and 72 hours, on 29 patients (11 of them did undergo myocardium revascularization with the application of EKC, while the rest of them did not). Activity of paraoxonase (both basal and activated) changes significantly during the postoperative period, in relation to pre-operative values, p < 0.05. Total cholesterol concentration is reduced in both examined groups, regardless of the application of EKC. This trend is also accompanied by LDL cholesterol concentration. On the other hand, HDL cholesterol concentration during post-operative period does not indicate any significant statistical change in relation to pre-operative values, while we noticed difference with regard to EKC application, 90 minutes after surgery. This change of lipid status indicator is partly due to heparin, a stimulator of lipoprotein lipase that was applied during the surgery. Our conclusion is that lipid profile changes significantly after the bypass surgery, mostly regardless of the application of EKC.     

Low density lipoproteins isolated from the blood of patients with ischemic heart disease induce accumulation of lipids in human aortic intima cells

Very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL) were isolated from the blood of healthy subjects and CHD patients. LDL from the blood of healthy individuals did not raise the intracellular lipid values within 24 h of cultivation. During intracellular lipid values within 24 h of cultivation. During the same incubation period. LDL obtained from the blood of CHD patients caused a 2- to 5-fold rise in cholesterol esters as well as a 1.5- to 3-fold rise in free cholesterol and triglycerides, while the intracellular phospholipid levels remained unchanged. In one of the three cases, the ability to raise the intracellular level of cholesterol esters was demonstrated by VLDL (500 micrograms/ml) derived from CHD patients blood. HDL did not affect the lipid levels in smooth muscle cells cultured from unaffected intima. The obtained data suggests that circulating LDL and, possibly, VLDL in the blood of CHD patients are capable of inducing the accumulation of fat in vascular wall cells.     

Lipoprotein, apolipoprotein, and lipolytic enzyme changes following estrogen administration in postmenopausal women

To test whether estrogen can modulate the cholesterolemic response to an Occidental diet, six healthy postmenopausal women were studied for 84 days while ingesting a solid food diet of constant composition high in cholesterol content (995 mg/d). In the middle of the study, estrogen (17 alpha-ethinyl estradiol, 1 microgram/kg per day) was administered orally. Ingestion of the diet for the initial 28 days did not alter lipoprotein lipid or apolipoprotein (apo) levels. However, with just 4 days of estrogen use there were significant decreases in apoE (-36%), low density lipoprotein cholesterol (-26%), and postheparin plasma hepatic triglyceride lipase activity (HTGL) (-61%), and an increase in high density lipoprotein (HDL) triglyceride (72%). These changes persisted throughout the estrogen use. The percent change in HTGL with 4 days of estrogen correlated inversely with the percent change in HDL triglyceride (rs = -0.94). After 28 days of estrogen there were also significant increases in HDL cholesterol (21%), HDL2 cholesterol (42%), apoA-I (37%), and apoA-II (9%), and a decrease in apoB (-11%). The level of apoE at this juncture correlated inversely with the level of HDL cholesterol (rs = -0.90), and the levels of HTGL and apoA-I correlated with HDL2 cholesterol (rs = -0.89 and rs = 0.89, respectively). Thus, HTGL may play a role in both the early estrogen-related changes in HDL triglyceride and apoE and the late estrogen-related changes in HDL cholesterol, apoA-I, and apoA-II.     

Antioxidant activity of high density lipoproteins in vivo]

The paper deals with antioxidant effect of high density lipoproteins (HDL) in vivo. The effect of intravenous injection of large-dose HDL3 (200 mg protein), isolated from human plasma to rabbits with experimental hypercholesterolemia, on the content of primary products of lipid peroxidation in rabbit blood, the correlation between HDL cholesterol level and the content of lipid peroxide products in blood plasma of healthy persons and patients with IHD were studied. Intravenous injection of HDL3 to rabbits with experimental hypercholesterolemia has been shown to lead in 6 hr to a 24-hr significant (p < 0.01) decrease of conjugated dienes and trienes. The existence of negative correlation between HDL-cholesterol level and the content of conjugated dienes in blood plasma of healthy persons (N = 47) and patients with IHD (n = 64) is revealed. Basing on the data obtained conclusion of universal character of protective antiatherogenic effect of HDL is drawn.     

Effect of apolipoprotein E-free high density lipoproteins on cholesterol metabolism in cultured pig hepatocytes

We studied cholesterol synthesis from [14C]acetate, cholesterol esterification from [14C]oleate, and cellular cholesterol and cholesteryl ester levels after incubating cells with apoE-free high density lipoproteins (HDL) or low density lipoproteins (LDL). LDL suppressed synthesis by up to 60%, stimulated esterification by up to 280%, and increased cell cholesteryl ester content about 4-fold. Esterification increased within 2 h, but synthesis was not suppressed until after 6 h. ApoE-free HDL suppressed esterification by about 50% within 2 h. Cholesterol synthesis was changed very little within 6 h, unless esterification was maximally suppressed; synthesis was then stimulated about 4-fold. HDL lowered cellular unesterified cholesterol by 13-20% within 2 h and promoted the removal of newly synthesized cholesterol and cholesteryl esters. These changes were transient; by 24 h, both esterification and cellular unesterified cholesterol returned to control levels, and cholesteryl esters increased 2-3-fold. HDL core lipid was taken up selectively from 125I-labeled [3H]cholesteryl ester- and ether-labeled HDL. LDL core lipid uptake was proportional to LDL apoprotein uptake. The findings suggest that 1) the cells respond initially to HDL or LDL with changes in esterification, and 2) HDL mediates both the removal of free cholesterol from the cell and the delivery of HDL cholesteryl esters to the cell.     

Influence of cholesterol status on blood lipid and lipoprotein enzyme responses to aerobic exercise.

To compare postexercise changes in plasma lipids and lipoprotein enzymes in 13 hypercholesterolemic (HC) and 12 normocholesterolemic men [total cholesterol (TC) 252 +/- 5 vs. 179 +/- 5 mg/dl], fasting blood samples were obtained 24 h before, immediately, 24, and 48 h after a single bout of treadmill walking (70% peak O(2) consumption, 500 kcal expenditure). Significant findings (P < 0.05 for all) for plasma volume-adjusted lipid and enzyme variables were that TC, low-density-lipoprotein cholesterol, and cholesterol ester transfer protein activity were higher in the HC group but did not influence the lipid responses to exercise. Across groups, TC was transiently reduced immediately after exercise but returned to baseline levels by 24 h postexercise. Decreases in triglyceride and increases in high-density-lipoprotein cholesterol (HDL-C) and HDL(3)-C were observed 24 h after exercise and lasted through 48 h. Lipoprotein lipase activity was elevated by 24 h and remained elevated 48 h after exercise. HDL(2)-C, cholesterol ester transfer protein activity, hepatic triglyceride lipase, and lecithin: cholesterol acyltransferase activities did not change after exercise. These data indicate that the exercise-induced changes in HDL-C and triglyceride are similar in HC and normocholesterolemic men and may be mediated, at least in part, by an increase in lipoprotein lipase activity.     

氧化修饰HDL对培养人主动脉平滑肌细胞胆固醇流出的影响

大量研究显示,高密度脂蛋白(highdensitylipoprotein,HDL)具有抗动脉粥样硬化(atherosclerosis,AS)作用.这是由于HDL能够促进外周组织如血管壁内皮细胞、平滑肌细胞(smoothmusclecell,SMC)及巨噬细胞储集的胆固醇流出,并将其转移到肝脏通过胆汁分泌而排出体外[1],这一过程...     

How soon after myocardial infarction should plasma lipid values be assessed?

Because acute myocardial infarction may affect plasma lipid concentrations it is commonly recommended that assessment of these concentrations should be delayed until about three months after the acute event. A study was therefore conducted of fasting plasma lipid concentrations in 58 patients with acute myocardial infarction. Measurements were made during their stay in hospital (days 1, 2, and 9) and three months later. Triglyceride concentrations remained unchanged throughout. Values of total cholesterol, low density lipoprotein, and high density lipoprotein all fell significantly between the first two days and day 9. Total cholesterol and low density lipoprotein also showed significant falls between days 1 and 2. Nevertheless, fasting plasma lipid concentrations showed no significant difference at any time during the first 48 hours from values measured three months later. After the infarction 26 patients changed to eating less fat or less energy, or both. More patients had hypercholesterolaemia in the first 48 hours than at three months. These results suggest that lipid state may be assessed as accurately, and possibly more accurately, during the first 48 hours after acute myocardial infarction than at three months.     

Free radical lipid oxidation affects cholesterol transfer between lipoproteins and erythrocytes

Human erythrocytes were incubated for 5 h at 37 degrees C with lipoproteins (LP), preliminary oxidized to different extent, as assessed by thiobarbituric acid (TBA) test. Cholesterol content in the cells was increased by 12-14% after incubation with low-density lipoproteins (LDL) along with augmentation of order parameter and rotational correlation time of spin-labeled stearic acids incorporated into membranes. If erythrocytes were incubated with oxidized LDL, containing 2.5-4 times more TBA-reactive material than native ones, cellular content of cholesterol was increased by 24-28%. In contrast, high-density lipoproteins (HDL2 and HDL3) removed cholesterol from cell membranes, when incubated with erythrocytes. This was followed by increased fluidity of membrane lipid phase as detected by the spin probe method. Oxidation of HDL2 and HDL3 decreased their ability to accept cholesterol from cell membranes. No detectable accumulation of TBA-reactive material was observed in the samples during the incubation. The antioxidant, butylated hydroxytoluene (BHT), in the concentration of 10(-5) M did not influence the cholesterol transfer between LP and erythrocytes. Hence, the effects of lipid peroxidation (LPO) on the cholesterol transfer seem to result from LP alterations by oxidation rather than from free radical reactions occurring during the incubation. By increasing cholesterol-donating ability of LDL and inhibition of cholesterol-accepting capacity of HDL lipid peroxidation in LP may activate cholesterol accumulation in blood vessel cells and thus contribute to atherosclerosis.     

Interrelation of the changes in the blood rheological properties and the microcirculatory disorders in the early and late stages of experimental hyperlipoproteinemia

Experiments were made on rabbit fed an atherogenic diet (0.5 g/kg cholesterol) singly for 15 and 24 h and repeatedly for 3, 9 and 30 days. At early stages of lipid metabolism distress the interrelationship was established between blood rheological disorders and microcirculatory abnormalities. The dependence of the initial reaction of some rheological characteristics on their initial level was marked.     

Effects of garlic extract consumption on blood lipid and oxidant/antioxidant parameters in humans with high blood cholesterol

Effects of garlic extract supplementation on blood lipid profile and oxidant/antioxidant status were investigated in volunteer subjects with high blood cholesterol. A total of 23 volunteer subjects with high blood cholesterol (>5.98 mmol/L) participated in the study. Of them, 13 patients were evaluated as a hypertensive group and the others a normotensive group. Before (first sample) and after (second sample) garlic extract consumption for 4 months, routine blood analyses including lipid parameters and liver and kidney function tests were performed. Additionally, blood oxidant (malondialdehyde [MDA], oxidation resistance [OR]), and antioxidant (antioxidant potential [AOP], nonenzymatic superoxide radical scavenger activity [NSSA]) parameters were measured. Serum total cholesterol, low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) cholesterols, and triglyceride levels were found to be significantly lowered, but HDL high-density lipoprotein cholesterol level increased after the extract use. The total:HDL cholesterol ratio was also found to be significantly decreased after the extract use. There were no meaningful differences with regard to other routine biochemical parameters. Additionally, blood AOP, OR, and NSSA values were found increased and MDA level decreased in the second samples relative to the first ones. Systolic and diastolic blood pressure values were also found to be significantly lowered after extract supplementation in the hypertensive group, but no similar changes were observed in the normotensive group. We conclude that garlic extract supplementation improves blood lipid profile, strengthens blood antioxidant potential, and causes significant reductions in systolic and diastolic blood pressures. It also leads to a decrease in the level of oxidation product (MDA) in the blood samples, which demonstrates reduced oxidation reactions in the body.     

HDL/LDL 比值、LP（a）及s-CRP 与冠脉病变程度相关性分析

目的:研究高密度脂蛋白/低密度脂蛋白比值(HDL/LDL比值)、脂蛋白a(LP(a))及超敏C反应蛋白(s-CRP)与冠脉病变程度之间的关系。方法:对120名初发急性STEMI行急诊冠脉造影术并支架植入术患者(<12小时),并于次日晨检测空腹生化血脂分析,测得HDL/LDL比值、LP(a)及s-CRP等相关指标,冠脉造影结果根据Gensini积分系统分轻、中、重度三组,比较三组之间上述三项指标有无差异,并选取冠脉造影正常20例为对照组,比较各组间有无差异。结果:与正常组相比,心梗组HDL/LDL比值明显降低(P<0.05),各组间HDL/LDL比值亦存在差异(P<0.05),LP(a)及s-CRP在不同冠脉分级上亦存在着差异(P<0.05),以上差异均有统计学意义。结论:上述三项指标对冠脉病变严重程度有一定的预测价值。     

Adrenergic mechanisms in control of plasma lipid concentrations.

The mechanisms of the changes in plasma lipids concentrations observed after beta-blockade were examined in 53 patients with hypertension receiving treatment with atenolol, metoprolol, propranolol, and oxprenolol in a randomised cross-over trial. Significant increases in mean plasma total and very-low-density lipoprotein (VLDL) triglyceride and reductions in high-density lipoprotein (HDL) cholesterol and free fatty acids concentrations wer observed with all four drugs, the increase in plasma triglyceride concentration being greatest after propranolol and oxprenolol. No significant changes were observed in total of LDL cholesterol concentrations, but HDL:LDL ratios and HDL cholesterol as a proportion of total cholesterol fell significantly. Thus plasma lipid concentrations should be monitored after three to six months of long-term treatment. Changes in triglyceride, HDL cholesterol and free fatty acid concentrations were associated with a highly significant reduction in clearance of soya oil (Intralipid) in 25 patients studied but were unrelated to changes in blood pressure. The fall in HDL cholesterol and rise in free fatty acid concentrations were significantly less in those with initially reduced HDL cholesterol or raised free fatty acid concentrations respectively. It is proposed that unopposed alpha stimulation inhibits lipoprotein lipase with a subsequent rise in plasma triglyceride and fall in HDL cholesterol concentration. Analysis of the relation between pretreatment concentrations and subsequent changes suggests that excessive alpha stimulation may impair production of HDL cholesterol in those with low HDL cholesterol concentrations before treatment. Subtle catecholamine-mediated changes in plasma lipid concentrations might provide a mechanism for the relation between stress and the development of cardiovascular events.     

Total and high-density lipoprotein cholesterol measurements. Hazards in clinical interpretation.

Duplicate plasma specimens from 24 persons were sent to a community hospital, a commercial laboratory, and a university lipid research laboratory at two separate times to assess the intralaboratory and interlaboratory variations of total and high-density cholesterol measurements. For all three laboratories, the 95% confidence limits for the reproducibility of total cholesterol levels are about +/- 5.5%. For high-density lipoprotein (HDL) values, they are +/- 7%, +/- 14.45%, and +/- 9%. Interlaboratory differences for total cholesterol at the 95% confidence level are +/- 7.7% and for HDL +/- 18.4%. Construction of a "cardiac risk ratio" of total to HDL cholesterol levels is subject to confusion because small errors in HDL cholesterol levels produce large errors in the ratio.     

SAA-only HDL formed during the acute phase response in apoA-I+/+ and apoA-I-/- mice.

Serum amyloid A (SAA) is an acute phase protein of unknown function that is involved in systemic amyloidosis and may also be involved in atherogenesis. The precise role of SAA in these processes has not been established. SAA circulates in plasma bound to high density lipoprotein-3 (HDL3). The pathway for the production of SAA-containing HDL is not known. To test whether apolipoprotein (apo)A-I-HDL is required in the production of SAA-HDL, we analyzed the lipopolysaccharide (LPS)-induced changes in apoA-I+/+ and apoA-I-/- mice. In apoA-I+/+ mice, after injection of LPS, remodeling of HDL occurred: total cholesterol increased and apoA-I decreased slightly and shifted to lighter density. Dense (density of HDL3) but large (size of HDL2 ) SAA-containing particles were formed. Upon fast phase liquid chromatography fractionation of plasma, >90% of SAA eluted with HDL that was enriched in cholesterol and phospholipid and shifted "leftward" to larger particles. Non-denaturing immunoprecipitation with anti-mouse apoA-I precipitated all of the apoA-I but not all of the SAA, confirming the presence of SAA-HDL devoid of apoA-I. In the apoA-I-/- mice, which normally have very low plasma lipid levels, LPS injection resulted in significantly increased total and HDL cholesterol. Greater than 90% of the SAA was lipid associated and was found on dense but large, spherical HDL particles essentially devoid of other apolipoproteins.We conclude that serum amyloid A (SAA) is able to sequester lipid, forming dense but large HDL particles with or without apoA-I or other apolipoproteins. The capacity to isolate lipoprotein particles containing SAA as the predominant or only apolipoprotein provides an important system to further explore the biological function of SAA.     

Effect of Metformin Treatment on Lipoprotein Subfractions in Non-Diabetic Patients with Acute Myocardial Infarction: A Glycometabolic Intervention as Adjunct to Primary Coronary Intervention in ST Elevation Myocardial Infarction (GIPS-III) Trial

Objective

Metformin affects low density lipoprotein (LDL) and high density (HDL) subfractions in the context of impaired glucose tolerance, but its effects in the setting of acute myocardial infarction (MI) are unknown. We determined whether metformin administration affects lipoprotein subfractions 4 months after ST-segment elevation MI (STEMI). Second, we assessed associations of lipoprotein subfractions with left ventricular ejection fraction (LVEF) and infarct size 4 months after STEMI.

Methods

371 participants without known diabetes participating in the GIPS-III trial, a placebo controlled, double-blind randomized trial studying the effect of metformin (500 mg bid) during 4 months after primary percutaneous coronary intervention for STEMI were included of whom 317 completed follow-up (clinicaltrial.gov Identifier: {"type":"clinical-trial","attrs":{"text":"NCT01217307","term_id":"NCT01217307"}}NCT01217307). Lipoprotein subfractions were measured using nuclear magnetic resonance spectroscopy at presentation, 24 hours and 4 months after STEMI. (Apo)lipoprotein measures were obtained during acute STEMI and 4 months post-STEMI. LVEF and infarct size were measured by cardiac magnetic resonance imaging.

Results

Metformin treatment slightly decreased LDL cholesterol levels (adjusted P = 0.01), whereas apoB remained unchanged. Large LDL particles and LDL size were also decreased after metformin treatment (adjusted P<0.001). After adjustment for covariates, increased small HDL particles at 24 hours after STEMI predicted higher LVEF (P = 0.005). In addition, increased medium-sized VLDL particles at the same time point predicted a smaller infarct size (P<0.001).

Conclusion

LDL cholesterol and large LDL particles were decreased during 4 months treatment with metformin started early after MI. Higher small HDL and medium VLDL particle concentrations are associated with favorable LVEF and infarct size.     

A Double-Blind, Placebo-Controlled Pilot Study to Evaluate the Effect of Calcium Fructoborate on Systemic Inflammation and Dyslipidemia Markers for Middle-Aged People with Primary Osteoarthritis

The objective of this pilot study was to determine whether 15?days of dietary supplementation with calcium fructoborate could acutely modulate inflammatory and lipid blood markers in individuals diagnosed with primary osteoarthritis. During 2?weeks, a placebo-controlled, randomized, double-blind study was conducted on 116 subjects that were initially recruited. Seventy-two subjects started the study, being divided into four groups, and only 60 completed the study as designed. The aim was to compare the effects of calcium fructoborate to placebo on subjects diagnosed with knee primary osteoarthritis. The obtained outcomes were inflammation biomarkers (C-reactive protein, fibrinogen, and erythrocyte sedimentation rate) and lipid markers (triglycerides, total cholesterol, LDL cholesterol, and HDL cholesterol). No serious adverse events were reported. The calcium fructoborate showed beneficial effect on the inflammatory markers for all groups subjected to the treatment when compared with the placebo group and slight changes in the lipid metabolism. This study suggests that short-term (2?weeks) calcium fructoborate supplementation in patients with osteoarthritis symptoms has a favorable prognosis on inflammation diseases.     

Association of increased oncostatin M with adverse left ventricular remodeling in patients with myocardial infarction

BackgroundThe study of laboratory biomarkers that reflect the development of adverse cardiovascular events in the postinfarction period is of current relevance. The aim of the present study was evaluation of oncostatin M (OSM) concentration changes in the early and late stages of myocardial infarction and evaluation of the possibility of its use in prediction of adverse left ventricular (LV) remodeling in patients with myocardial infarction with ST-elevated segment (STEMI).MethodsThe study involved 31 patients with STEMI admitted in the first 24 hours after the onset of MI and 30 patients with chronic coronary artery disease as a control group. Echocardiographic study was performed on day 3 and in 6 months after STEMI. The serum levels of biomarkers were evaluated on the day of hospital admission and 6 months after MI using multiplex immunoassay.ResultsOSM level increased during the first 24 h after the onset of the disease, with the following decrease in 6 months. OSM concentration at admission had correlated with echocardiography parameters and Nt-proBNP, troponin I, CK-MB levels. Our study has demonstrated association of the increased levels of OSM at the early stages of STEMI with development of the adverse LV remodeling in 6 months after the event.ConclusionsElevation of OSM levels in the first 24 h after STEMI is associated with the development of the adverse LV remodeling in the long-term post-infarction period.     

Effects of interleukin-2 (IL-2) on human plasma lipid,lipoprotein, and C-reactive protein

Six patients with confirmed malignant disease received four consecutive weekly cycles of human recombinant interleukin-2 (IL-2) 4 days/week, continuous iv. infusion, 3 × 10⁶ U/m²/day. Plasma cholesterol decreased a mean of 7% within 24 hours after IL-2 infusion and decreased by 33% within 4 days. Plasma cholesterol was significantly lower than baseline concentration by day 21 (–21%), and day 25 (–41%) was significantly lower than day 21. Decreased plasma cholesterol was the result of decreased HDL and LDL cholesterol concentrations. Plasma triglyceride demonstrated a mean increase of 46% after 4 days of therapy and remained greater than baseline concentrations at all time points analyzed. Apolipoprotein AI and AII decreased concomitantly with HDL-cholesterol concentrations, whereas apolipoprotein B after an initial mean decrease of 17% during the first cycle was not significantly different from baseline during the fourth cycle. Apolipoprotein E and Lp(a) were not significantly affected by IL-2 treatment. Plasma C-reactive protein (CRP) increased by 79% within 24 hours of therapy, increased by 254% on day 4, then decreased to baseline concentrations by day 21 after 3 days off of IL-2. Day 25 CRP was elevated compared to both baseline and day 21 concentrations. IL-2 induced plasma lipoprotein changes may be due in part to the induction of interferon gamma.