Postprandial lipemia in postmenopausal women with high fasting high-density lipoprotein cholesterol

BACKGROUND: Several groups of patients at high risk for cardiovascular disease have been found to show an exaggerated postprandial hypertriglyceridemia. Postprandial lipemia (PPL) therefore has been implicated as a potential additional risk factor that has been evading us. The purpose of this study was to test the effect of high fasting high-density lipoprotein cholesterol (HDL-C) levels on PPL in postmenopausal females. METHODS: Oral fat tolerance test, as quantified by the areas under the curve (AUC) of triglyceride (TG) levels, was given to 3 groups: normal postmenopausal females (control), postmenopausal females with exceptionally high HDL-C and a familial history of longevity (longevity syndrome), and postmenopausal females that were heterozygotes of familial hypercholesterolemia (hFH) with exceptionally high HDL-C. RESULTS: The PPL was not different between the control and longevity syndrome groups but was significantly higher in the hFH group; AUC (SD), in mg/dl/h; 749 (195), 882 (278) and 1244 (497) respectively, p=0.002. In linear regression analysis only fasting TG levels were a significant predictor of the AUC (Coefficient B = 11.779, p < 0.001). CONCLUSIONS: In subjects with longevity syndrome the PPL is similar to controls, which means that high fasting HDL-C has not any beneficial influence on PPL. The fasting TG concentration is the main determinant of PPL. Furthermore, postmenopausal females with hFH have higher TG response postprandially, even in the case of high fasting HDL-C. Whether there is a threshold below or above, where HDL-C becomes a significant independent determinant of PPL is a question to be answered by future research.     

Influence of mild to moderately elevated triglycerides on low density lipoprotein subfraction concentration and composition in healthy men with low high density lipoprotein cholesterol levels

Epidemiologic studies have shown that a dyslipoproteinemia with low concentrations of high density lipoprotein (HDL) cholesterol and elevated serum triglycerides (TG) is associated with a particularly high incidence of coronary artery disease. This lipid profile is associated with increased concentrations of small, dense low density lipoprotein (LDL) particles. To evaluate the role of mild to moderately elevated TG on the LDL subfraction profile in patients with low HDL cholesterol, concentration and composition of six LDL subfractions was determined by density gradient ultracentrifugation in 41 healthy men (31+/-9 years, body mass index (BMI) 25.1+/-3.9 kg/m2) with equally low HDL cholesterol levels < 0.91 mmol/l but different TG levels: TG < 1.13 mmol/l, n = 16; TG = 1.13-2.26 mmol/l, n = 13: TG = 2.26-3.39 mmol/l, n = 12. Those men with moderately elevated TG levels between 2.26 and 3.39 mmol/l had significantly higher concentrations of very low density lipoprotein (VLDL), intermediate low density lipoprotein (IDL), and small, dense LDL apoB and cholesterol than men with TG < 1.13 mmol/l. With increasing serum TG, the TG content per particle also increased in VLDL, IDL as well as total LDL particles while the cholesterol and phospholipid (PL) content decreased in VLDL and IDL, but not in LDL particles. LDL subfraction analysis revealed that only large, more buoyant LDL particles (d < 1.044 g/ml) but not the smaller, more dense LDL, were enriched in TG. Small, dense LDL particles were depleted of free cholesterol (FC) and PL. This study has shown that in men with low HDL cholesterol levels mild to moderately elevated serum TG strongly suggest the presence of other metabolic cardiovascular risk factors and in particular of a more atherogenic LDL subfraction profile of increased concentration of small, dense LDL particles that are depleted in surface lipids.     

Prednisone increases very low density lipoprotein and high density lipoprotein in healthy men

To determine the effect of corticosteroids on lipoprotein metabolism in healthy subjects, we measured lipoprotein lipid and apoprotein levels in eight normolipidemic healthy men before, during, and after administration of oral prednisone 0.35 mg/kg/d. After 14 days of prednisone, there was a significant increase in levels (mg/dL) of very low density lipoprotein-triglyceride (VLDL-TG) (51 +/- 9 v 92 +/- 11, P less than .01), very low density lipoprotein-cholesterol (VLDL-C) (19 +/- 2 v 28 +/- 3, P less than .01), high density lipoprotein-cholesterol (HDL-C) (39 +/- 1 v 50 +/- 4, P less than .05), apolipoprotein (apo) AI (124 +/- 7 v 147 +/- 8, P less than .01), and apo E (3.1 +/- 0.4 v 4.1 +/- 0.4, P less than .01). In addition, the activity of lipoprotein lipase but not hepatic lipase in postheparin plasma also was higher after prednisone treatment. All values returned to baseline within 2 weeks after discontinuation of prednisone. Short-term administration of corticosteroids has a consistent effect on the metabolism of both VLDL and HDL.     

Inverse relationship between blood levels of high density lipoprotein subfraction 2 and magnitude of postprandial lipemia.

Triglyceridemic response to a standard oral fat meal was determined in 28 healthy subjects and related to the levels of several lipids, lipoproteins, and apolipoproteins in the post-absorptive plasma. A fatty test meal was administered orally, and postprandial plasma triglyceride levels were determined. In the fasting blood samples, concentrations of apolipoproteins (apo) A-I, A-II, and B were determined by radioimmunoassay, and those of high density lipoprotein (HDL) subfractions HDL2 and HDL3, by zonal ultracentrifugation. The magnitude of triglyceridemic response showed a negative correlation with the plasma levels of HDL2 (r = -0.860, P less than 0.001), HDL-associated cholesterol (r = -0.605, P less than 0.001), and apoA-I (r = -0.459, P less than 0.02). No correlation was found between the triglyceridemic response and the levels of total cholesterol, HDL3, and apoA-II. Triglyceridemic response was correlated positively with fasting triglyceride concentrations (r = 0.450, P less than 0.02) and apoB levels (r = 0.396, P less than 0.03). In two subjects followed for 3 yr, when HDL2 levels rose or fell, the triglyceridemic response decreased or increased, respectively (r = -0.944; r = -0.863). Our data indicate that normolipidemic individuals with high HDL2 levels in the plasma are able to clear alimentary fat at a faster rate than normolipidemic subjects with low HDL2 levels. The pronounced difference in severity and duration of postprandial lipemia among subjects with varying HDL2 levels may help to explain the negative correlation between the risk of atherosclerosis and HDL cholesterol levels.     

Seasonal variation of serum high density lipoprotein cholesterol levels in men

To determine if there are seasonal variations in serum high density lipoprotein cholesterol (HDL-C), the concentration of HDL-C was measured monthly for 12 consecutive months in 31 healthy men and 24 male inpatients with schizophrenia. In addition to HDL-C, total cholesterol (TC) and triglyceride (TG) concentrations in serum were assayed, and low density lipoprotein cholesterol (LDL-C) was estimated by calculation. Mean serum HDL-C levels of schizophrenic patients were significantly low compared with those of healthy controls, 35 +/- 12 and 49 +/- 11 mg/dl, respectively. The TC levels of schizophrenic patients were significantly higher in January and March as compared with August. The HDL-C levels in summer and autumn were significantly lower than those in winter and spring in both healthy men and schizophrenic patients. The concentration of LDL-C was significantly high in September and October as compared with April in healthy men. In patients with schizophrenia, LDL-C level seemed higher in January and March as compared with August.     

Elevated high density lipoprotein cholesterol and low grade systemic inflammation is associated with increased gut permeability in normoglycemic men

Background & aims

Serum lipids and lipoproteins are established biomarkers of cardiovascular disease risk that could be influenced by impaired gut barrier function via effects on the absorption of dietary and biliary cholesterol. The aim of this study was to examine the potential relationship between gut barrier function (gut permeability) and concentration of serum lipids and lipoproteins, in an ancillary analysis of serum samples taken from a previous study.

Sex differences in high density lipoprotein cholesterol among low-level alcohol consumers

The purpose of this study was to examine high density lipoprotein cholesterol (HDL-C) levels in a sample of community-living women and men who consumed 1 drink of alcohol/day or less. Self-reports of alcohol consumption and clinical assessments of plasma lipid and lipoprotein levels were obtained twice, at 12 months apart. Among men, consumption of 1 drink/day or less was unrelated to levels in HDL-C. In contrast, among women alcohol consumption throughout this relatively low consumption range was positively associated with HDL-C levels. These findings indicate that the association of alcohol and higher levels of HDL-C may occur at lower intakes of alcohol in women than in men.     

Effect of weight loss on postprandial lipemia and low-density lipoprotein receptor binding in overweight men

Obestity is associated with a range of metabolic abnormalities including fasting and postprandial dyslipidemia, both of which may contribute to increased atherosclerotic risk. Male obese subjects have a decreased level of low-density lipoprotein (LDL) receptor binding in mononuclear cells, the level of which reflects binding in the liver, compared with lean controls. In this study, we investigated whether the implementation of a weight loss regimen in viscerally obese subjects improves LDL receptor binding level. We examined apolipoprotein B(48) (apo B(48)) and retinyl palmitate (RP) metabolism following an oral fat challenge to determine whether weight loss improves postprandial dyslipidemia in viscerally obese subjects. Male obese, mildly dyslipidemic, and insulin-resistant subjects were randomly assigned to either a weight loss (n = 12) or control weight maintenance (n = 10) group. In response to weight loss of 10 kg, insulin sensitivity improved as evidenced by decreased fasting insulin and homeostatic model assessment (HOMA) score. In addition, LDL receptor binding in mononuclear cells increased significantly by 27.5% and LDL-cholesterol was significantly reduced. However, despite the increased LDL receptor levels, fasting apo B(48) levels did not fall. Postprandially, the area under the curve (AUC) for RP was significantly reduced after weight loss, but the incremental and total AUCs for apo B(48) were not altered. Apo B(48) is an unequivocal marker of chylomicron particle number; hence, the reduction in RP metabolism achieved with weight reduction may reflect decreased lipid incorporation into nascent chylomicrons or improved hydrolysis of triglyceride-rich chylomicrons resulting from a decreased competition with hepatic lipoproteins for lipoprotein lipase. Our findings suggest that the improvement in LDL receptor binding following weight reduction of 10 kg in insulin-resistant male obese subjects is insufficient to reduce the elevated chylomicron remnant levels.     

Low dose continuously infused growth hormone results in increased lipoprotein(a) and decreased low density lipoprotein cholesterol concentrations in middle-aged men

OBJECTIVE Animal studies have shown that slight increases in basal GH concentrations may result in changes in lipoprotein metabolism. Such changes in GH secretion have been observed in physiological and pathophysiological states such as fasting, uncontrolled diabetes and during oestrogen treatment. The aim of this study was to investigate the possible effects of increases in basal plasma GH concentrations on lipoprotein concentrations. DESIGNS Recombinant human growth hormone (rhGH) was given as a continuous subcutaneous infusion in a low dose (0.02 U/kg/day) in an open study. PATIENTS Eight middle-aged (42–59 years) overweight (body mass index: 26.1–33.8 kg/m²) but otherwise healthy men were studied over a period of 14 days. MEASUREMENTS Blood samples were obtained after an over-night fast before and after 2, 7 and 14 days of treatment. Plasma and serum were separated and used for subsequent measurements of hormone and lipoprotein concentrations. On days 0, 7 and 14 of treatment, post-heparin plasma was also obtained for determinations of plasma lipoprotein lipase and hepatic lipase activities. In addition, a hyperinsuiinaemic euglycaemic glucose clamp was performed on days 0 and 13 of the study. Fat biopsies from abdominal and gluteal fat depots were obtained for measurement of lipoprotein lipase activities on days 0 and 14 of the study. RESULTS Serum GH concentrations increased to a steady level of 2–4mU/l during treatment. Serum insulin-like growth factor-l (IGF-I) concentrations increased throughout the treatment period to twice the pretreatment levels. Plasma insulin and blood glucose concentrations increased on day 2 of treatment. After 7 and 14 days of treatment blood glucose concentrations were not different from pretreatment levels, but plasma insulin concentrations were still elevated. Serum cholesterol and low density lipoprotein (LDL) cholesterol concentrations had decreased after 7 and 14 days of treatment. High density lipoprotein (HDL) cholesterol concentrations were not affected, but very low density lipoprotein (VLDL) cholesterol and triglyceride concentrations increased transiently at day 2 of treatment. Serum apolipoprotein (apo) A-l, apoB and apoE concentrations were not significantly affected. Serum lipoprotein(a) concentrations had increased by days 7 and 14 to 147 and 142% of pretreatment concentrations, respectively. Lipoprotein lipase and hepatic lipase activities in post-heparin plasma, as well as abdominal and gluteal adipose tissue lipoprotein lipase activities, were not affected. There was no significant change in glucose disposal rate estimated from the glucose clamp studies. CONCLUSIONS A low dose infusion of GH results in marked changes in lipoprotein concentrations with a transient increase in VLDL cholesterol and thereafter in a decrease in LDL cholesterol. In addition, this low dose of GH resulted in marked increases in lipoprotein(a) concentrations. The observed effects of GH may partly involve changes in IGF-I and insulin secretion.     

Relation between high density lipoprotein cholesterol and coronary artery disease in asymptomatic men

The well established inverse relation of high density lipoprotein cholesterol (HDL) and the risk of coronary artery disease was tested in a cross-Sectional group of 572 asymptomatic aircrew members who were being screened for risk of coronary artery disease. A battery of tests was performed, including determinations of fasting serum cholesterol, HDL cholesterol and triglycerides and performance of a maximal symptomlimited exercise tolerance test. Of the 572 patients, 132 also had an abnormal S-T segment response to exercise testing or were otherwise believed to have an increased risk of organic heart disease and subsequently underwent coronary angiography. Significant coronary artery disease was found in 16 men and minimal or subcritical coronary disease in 14; coronary angiograms were normal in the remaining 102 men. The remaining 440 men, who were believed to have a 1 percent chance of having coronary artery disease by sequential testing of risk factors and treadmill testing, had a mean cholesterol level of 213 mg/100 ml, a mean HDL cholesterol of 51 mg/100 ml and a mean cholesterol/HDL ratio of 4.4. The mean values for cholesterol, HDL cholesterol and cholesterol/HDL cholesterol did not differ significantly in men with normal angiographic findings and those with subcritical coronary disease. However, 14 of 16 men with coronary artery disease had a cholesterol/HDL ratio of 6.0 or more whereas only 4 men with normal coronary arteries had a ratio of 6.0 or more. Of the classic coronary risk factors evaluated, the cholesterol/HDL ratio of 6.0 or more had the highest odds ratio (172:1). It appears that determination of HDL cholesterol level helps to identify asymptomatic persons with a greater risk of having coronary artery disease.     

Benefits of lipid-lowering therapy in men with elevated apolipoprotein B are not confined to those with very high low density lipoprotein cholesterol

Objectives. Do the benefits of intensive lipid-lowering therapy extend to patients with only borderline or moderately elevated levels of low density lipoprotein (LDL) cholesterol?Background. The merits of the present LDL cholesterol treatment goal of ≤100 mg/dl need to be clarified for patients without high levels of LDL cholesterol, particularly for those patients previously classified as having only borderline high (130 to 159 mg/dl) or desirable (101 to 130 mg/dl) levels.Methods. Disease change and clinical events were examined in LDL cholesterol subgroups in the Familial Atherosclerosis Treatment Study (FATS) trial, a randomized, blinded, quantitative arteriographie comparison of one conventional and two intensive lipid-lowering strategies in men with coronary artery disease, a positive family history and apolipoprotein B ≥125 mg/dl. The primary end point, disease change per patient, was measured as the mean change in severity of stenosis (Δ%S_Prox) among nine standard proximal segments.Results. Of the 120 patients completing the 30-month protocol, 60 had a baseline LDL cholesterol <90th percentile (mean LDL cholesterol 152 mg/dl) and 60 >90th percentile (mean LDL cholesterol 221 mg/dl). Thirty-one patients had levels <160 mg/dl (mean LDL cholesterol 134 mg/dl) and 89 >160 mg/dl (mean LDL cholesterol 205 mg/dl). Patients with LDL cholesterol <90th percentile benefited angiographically from therapy (Δ%S_Prox= −1.5% diameter stenosis [regression] during intensive therapy vs. 4-2.3% diameter stenosis [progression] during conventional therapy, p < 0.01), as did patients with LDL cholesterol <160 mg/dl (Δ%S_Prox= −4.2% vs. +3.3% diameter stenosis, p = 0.0001). By comparison, angiographie benefit was less pronounced among those entdring with very high LDL cholesterol (Δ%S^Prox= −0.2% vs. +1.9% diameter stenosis, p = 0.07) or with LDL cholesterol ≥160 mg/dl (Δ%S_Prox= +0.2% vs. +1.6% diameter stenosis, p = 0.13). Intensive therapy resulted in a statistically significant reduction in clinical events only in the subgroup with baseline LDL cholesterol < 90th percentile (2 of 42 vs. 8 of 29 patients initially enrolled, p = 0.01) and a trend toward fewer events in patients with LDL cholesterol < 160 mg/dl (2 of 20 vs. 6 of 15 patients, p = 0.05). No such difference was seen in the higher LDL cholesterol subgroups.Conclusions. Treatment benefit in the FATS trial was not confined to patients with very high levels of LDL cholesterol and was in fact particularly evident in those patients with levels < 160 mg/dl. Such patients should be considered more likely, not less, to benefit from intensive lipid-lowering therapy.     

Seasonal variation in high density lipoprotein cholesterol

We investigated the seasonal variation in high density lipoprotein cholesterol (HDL) in 142 dyslipidemic (non-HDL-cholesterol ≥ 5.2 mmol/1) middle-aged men in the placebo group of the Helsinki Heart Study over the 5-year trial period. A seasonal pattern was found in HDL fluctuation, with a 4.5% drop during mid-winter (5-year mean 1.192 ± 0.265 mmol/1) compared with a stable level (5-year mean 1.248 ± 0.281 mmol/1) during the rest of the year (P < 0.001). A less pronounced seasonal variation in HDL was observed in 85 subjects receiving gemfibrozil. Although affecting pretrial HDL level in cross-sectional analyses, age, alcohol consumption, dietary adherence, physical activity and serum triglycerides had no influence on the seasonality of HDL variation. Smoking had a slight attenuating effect on the variation pattern. Pretrial HDL was influenced by relative weight, but there was also an inverse relationship between HDL and body weight variations, i.e. the annual drop in HDL coincided with the annual peak in body weight. However, seasonal HDL variation was not directly reflected in the annual variation in CHD incidence.     

Relationship between plasma insulin levels and high density lipoprotein cholesterol levels in healthy men

Summary Insulin and high density lipoproteins are considered to play a role in the development of atherosclerosis. In order to study whether there was a relationship between endogenous plasma insulin response and high density lipoproteins, an acute intravenous glucose tolerance test (0.5 g glucose/kg body weight) was performed in 94 healthy men, aged 20–49 years. Cholesterol and triglyceride levels were measured in very low density lipoproteins, low density lipoproteins and high density lipoproteins isolated from fasting serum by preparative ultracentrifugation. The subjects were divided into quartiles according to their fasting and post-glucose load plasma insulin and high density lipoprotein cholesterol levels. The results obtained in the subjects of the upper quartiles were compared with the results obtained in the subjects of the lower quartiles. The mean glucose disappearance rates were within the normal range and did not differ between the upper and lower quartiles. Subjects with high fasting plasma insulin had lower high density lipoprotein cholesterol levels (1.11±0.34 mmol/l, p=0.01) than men with low fasting plasma insulin (1.40±0.37 mmol/l). Higher mean post-glucose plasma insulin was associated with lower high density lipoprotein cholesterol levels (1.18±0.32 mmol/l, p<0.05) and increased high density lipoprotein triglyceride levels (0.14±0.07 mmol/l, p<0.01) when compared with the men with low post-glucose plasma insulin (1.40±0.36 mmol/l and 0.09±0.03 mmol/l respectively). These observations reflect the close relationship between endogenous insulin and lipoprotein metabolism.     

Reduction of high density lipoprotein cholesterol and apoliproprotein A-I concentrations by a lipid-lowering diet

Nine hyperlipoproteinaemic patients were treated with a serum lipid-lowering diet during 4 weeks in a metabolic ward. The diet contained 35% energy from fat and the ratio between polyunsaturated and saturated fats (the P/S ratio) was 2.0. This treatment caused a reduction of the serum concentrations of the low density lipoprotein cholesterol (Chol) by 17% (P less than 0.01), of the apolipoprotein (apo) B by 27% (P less than 0.01), of high density lipoprotein (HDL) Chol by 15% (P less than 0.05) and of the apo A-I by 9% (P less than 0.02). The apo B/apo A-I ratio decreased by 19% (P less than 0.01). It is suggested that the reduced HLD Chol and apo A-I concentrations may be due to both the qualitative change to more polyunsaturated fats in the diet and to the reduction of the total dietary fat intake.     

Alfalfa seeds lower low density lipoprotein cholesterol and apolipoprotein B concentrations in patients with type II hyperlipoproteinemia

Fifteen patients with hyperlipoproteinemia (HLP), types IIA (n = 8), IIB (n = 3) and IV (n = 4) were given 40 g of heat prepared alfalfa seeds 3 times daily at mealtimes for 8 weeks with otherwise unchanged diet. In patients with type II HLP alfalfa treatment caused after 8 weeks a maximal lowering of pretreatment median values of total plasma cholesterol from 9.58 to 8.00 mmol/l (P less than 0.001) and low density lipoprotein (LDL) cholesterol from 7.69 to 6.33 mmol/l (P less than 0.01), which corresponds to decreases of 17% and 18%, respectively. Maximal decrease was 26% in total cholesterol and 30% in LDL cholesterol. In two patients with hypercholesterolemia the LDL cholesterol decreased less than 5%. Apolipoprotein B decreased in the same period from 2.17 to 1.43 g/l (P less than 0.05) in type II HLP, corresponding to 34% decrease, whereas apolipoprotein A-I did not change. Body weight increased slightly during the first 4 weeks of alfalfa treatment (P less than 0.001) probably because of the caloric content in the alfalfa seeds. After cessation of treatment, all lipoprotein concentrations returned to pretreatment levels. We conclude that alfalfa seeds can be added to the diet to help normalize serum cholesterol concentrations in patients with type II HLP.     

Decreased high density lipoprotein cholesterol in hypopituitarism.

Serum triglyceride, cholesterol, and high density lipoprotein cholesterol (HDL-C) levels were measured in 10 men and 3 women with hypopituitarism. The mean total cholesterol and triglyceride levels were significantly increased but were within the range of controls. The mean HDL-C concentration and the HDL-C to total cholesterol ratio were significantly decreased. Similar findings were present in a patient with isolated GH deficiency. Two men with Kallman's syndrome and 3 patients with active acromegaly had values that were either within or just below the normal range. Replacement therapy with thyroid hormone and prednisone resulted in a normalization of HDL-C concentrations in four of the five patients studied. This improvement suggests a role for thyroid hormone and/or glucocorticoids in the maintenance of normal HDL-C concentrations. These observations also suggest that the distribution of plasma lipoprotein fractions is dependent in part, either directly or indirectly, on pituitary hormones.     

血清小而密低密度脂蛋白胆固醇、同型半胱氨酸与颈动脉粥样硬化关系研究

目的探讨血清小而密低密度脂蛋白胆固醇(sdLDL-C),小而密低密度脂蛋白胆固醇与低密度脂蛋白胆固醇之比(sdLDL-C/LDL-C)及同型半胱氨酸(Hcy)与颈动脉硬化的关系,并分析sdLDL-C/LDL-C评价颈动脉斑块的价值。方法选取2017年10月至2019年10月于安徽医科大学合肥第三临床学院心内科住院并行颈动脉彩超检查的200例患者为研究对象,根据颈动脉超声结果分为颈动脉内膜中层厚度(IMT)异常组(n=122)和对照组(n=78)。其中,IMT异常组又分为IMT增厚组(n=30)及颈动脉斑块组(n=92)。Spearman相关分析sdLDL-C与年龄、体质指数(BMI)、LDL-C、高密度脂蛋白胆固醇(HDL-C)、sdLDL-C/LDL-C、超敏C反应蛋白(hs-CRP)、Hcy的相关性;二元Logistic逐步回归方程及有序多分类Logistic回归模型评估颈动脉斑块的独立危险因素。结果IMT异常组血清sdLDL-C、sdLDL-C/LDL-C和Hcy水平均明显高于对照组,差异有统计学意义(P<0.05)。颈动脉斑块组血清sdLDL-C、sdLDL-C/LDL-C和Hcy水平均明显高于IMT增厚组,差异亦均有统计学意义(P<0.001)。Logistic逐步回归分析显示年龄、糖尿病、Hcy、sdLDL-C/LDL-C、sdLDL-C是IMT增厚和颈动脉斑块的独立危险因素。结论在伴有IMT增厚、颈动脉斑块患者中sdLDL-C、sdLDL-C/LDL-C、Hcy水平显著升高。血清sdLDL-C/LDL-C、sdLDL-C、Hcy含量具有颈动脉斑块的预测价值,且是颈动脉粥样硬化的独立危险因素。     

Relationship of high density lipoprotein composition to plasma lecithin:cholesterol acyltransferase concentration in men

The epidemiological associations between the plasma concentrations of several components of high density lipoprotein (HDL) and plasma lecithin:cholesterol acyltransferase (LCAT) concentration have been studied in 101 men aged 52-67 years. Subjects were apparently healthy, and had been selected to provide a wide range of HDL-cholesterol levels. A weak positive correlation was observed between plasma total HDL-cholesterol concentration and LCAT concentration (r = 0.24, P less than 0.02). This reflected an association between HDL3-cholesterol (measured by precipitation) and enzyme concentration (r = 0.21, P less than 0.05). Apoprotein (apo) A-II concentration was also positively correlated with LCAT (r = 0.27, P less than 0.01). HDL2-cholesterol and apo A-I concentration were unrelated to LCAT concentration, as also were the HDL2/HDL3 and HDL-cholesterol/apo A-I ratios. The associations of HDL3 cholesterol and apo A-II with LCAT were strengthened when allowance was made by multiple regression for the effect of log plasma triglyceride; under these circumstances variation in LCAT explained statistically 8% of the variance in HDL3-cholesterol, and 10% of that in apo A-II.     

Plasma testosterone,high density lipoprotein cholesterol and other lipoprotein fractions

High density lipoprotein (HDL) cholesterol levels are strongly related to risk of heart attack. Identification of determinants of high density lipoprotein cholesterol may provide important information concerning the cause of heart disease. The relation between one possible determinant, testosterone, and high density lipoprotein cholesterol and other lipoprotein fractions was evaluated in 247 middle-aged men. The results indicate that testosterone levels (both free and total) were positively correlated with high density lipoprotein cholesterol (r = +0.24, p < 0.01) and negatively correlated with triglycerides and very low density lipoprotein cholesterol. The association between testosterone and high density lipoprotein cholesterol could not be explained by intake of alcohol, obesity, age, smoking or physical activity. Furthermore, the relation of testosterone to HDL cholesterol was independent of the relation of testosterone to very low density lipoprotein (VLDL) cholesterol or triglycerides.