香蕉抗脂蛋白氧化修饰作用的研究

目的研究香蕉的抗血浆脂蛋白氧化作用.方法 20名健康受试者空腹食用新鲜香蕉后抽取静脉血,采用序列超速离心法分离血浆极低密度脂蛋白(VLDL)、低密度脂蛋白(LDL)和高密度脂蛋白(HDL),并观察各血浆脂蛋白过氧化程度以及氧化易感性的变化.结果香蕉食用后受试者血浆VLDL、LDL和HDL过氧化脂质水平明显降低,分别减少29%、25%和30%;在体外进行氧化修饰时,LDL氧化延滞时间明显延长,从(64±29)min延长至(83±36)min,提示LDL氧化易感性下降.结论新鲜香蕉可降低脂蛋白过氧化程度和增强LDL抗氧化修饰能力,因此能够起到防治心血管疾病的积极作用.     

大豆异黄酮对糖尿病大鼠脂蛋白氧化的影响

目的 研究大豆异黄酮对糖尿病大鼠血浆脂蛋白脂质过氧化的影响。方法 给糖尿病大鼠饲喂添加大豆异黄酮的饲料8周，检测其血浆脂蛋白过氧化脂质程度以及氧化易感性的变化。结果 食用大豆异黄酮的糖尿病大鼠血浆总过氧化脂质低密度脂蛋白(LDL)和高密度脂蛋白(HDL)过氧化脂质含量明显减少，且在体外进行氧化修饰时，LDL氧化延滞时间明显延长，提示LDL氧化易感性下降。结论 大豆异黄酮显降低糖尿病大鼠LDL和HDL脂质过氧化程度，降低LDL氧化易感性，对糖尿病及其并发症的发生和发展能起到有效的防治作用。     

大豆胚轴对糖尿病大鼠脂蛋白氧化拮抗作用

目的 研究大豆胚轴提取物对糖尿病大鼠血浆脂蛋白氧化的抑制作用.方法 从大豆胚轴提取总糖甙,高效液相色谱法(HPLC)分析其有效成分.给糖尿病大鼠饲喂添加100 g/kg大豆胚轴提取物的饲料20周,观察血浆脂蛋白过氧化脂质(LPO)含量及氧化易感性的变化.结果 饲喂大豆胚轴提取物后实验组糖尿病大鼠血浆LPO、低密度脂蛋白(LDL)-LPO和高密度脂蛋白(HDL)-LPO分别为(17.1±2.2),(2.6±0.5),(3.9±0.7)μmol/L,较对照组大鼠(21.4±3.5)、(3.4±0.8)和(5.4±0.9)μmol/L明显减少;在体外进行氧化修饰时,实验组大鼠LDL氧化延滞时间为(120±36)min,较对照组大鼠(83±27)min明显延长.结论 大豆胚轴提取物可降低脂蛋白过氧化程度和增强LDL抗氧化修饰能力,有防治糖尿病及其并发症的作用.     

脂蛋白与高脂蛋白血症

血浆脂蛋白由蛋白质、甘油三酯、磷脂、胆固醇及胆固醇酯组成，可分为乳糜微粒（CM）、极低密度脂蛋白（VLDL）、低密度脂蛋白（LDL）、中间密度脂蛋白（IDL）及高密度脂蛋白（HDL）五种。     

脂蛋白与高脂蛋白血症

血浆脂蛋白由蛋白质、甘油三酯、磷脂、胆固醇及胆固醇酯组成,可分为乳糜微粒(CM)、极低密度脂蛋白(VLDL)、低密度脂蛋白(LDL)、中间密度脂蛋白(IDL)及高密度脂蛋白(HDL)五种。     

脂蛋白在脂多糖诱导THP-1细胞活化中的调节机制

目的 研究血清脂蛋白对脂多糖的影响机制,并对不同种类脂蛋白:高密度脂蛋白(HDL)、低密度脂蛋白(LDL)和极低密度脂蛋白(VLDL),抑制脂多糖的能力进行比较,为研究脂蛋白在治疗败血症中的应用提供理论基础.方法 通过检测经佛波醇酯刺激分化的THP-1细胞分泌的TNF-α间接反映脂蛋白对脂多糖的抑制作用.将不同浓度脂多糖与THP-1细胞在血清基质中混合孵育4 h,并与3种脂蛋白-脂多糖混合液与THP-1细胞混合孵育后TNF-α的分泌量进行对比,计算脂蛋白对脂多糖的抑制情况.结果 HDL、LDL和VLDL单独不能诱导分化的THP-1细胞分泌TNF-α(P＞0.05).当10 ng/mL脂多糖与0.05 mg/m以上浓度的脂蛋白(HDL、LDL和VLDL)混合时,TNF-α分泌量明显降低.当脂多糖浓度为100 ng/mL时,0.1 mg/mL的脂蛋白(HDL、LDL和VLDL)对其抑制效果较低,分别为(20.7±11.1)%、(8.9±2.8)%、(4.3±1.6)%;在脂多糖浓度为10 ng/mL抑制效果明显增强,抑制率分别为(69.3±3.7)%、(42.9±5.7)%、(42.7±4.5)%.HDL对各浓度脂多糖的抑制效果均强于LDL和VLDL(P＜0.05).结论 脂蛋白在血清中能抑制脂多糖活化巨噬细胞分泌细胞因子,但抑制效果在脂多糖浓度高时相比浓度低时差.HDL对脂多糖活化巨噬细胞的抑制作用比LDL和VLDL强.     

原发性高胆固醇血症的发病机理

大多数原发性高胆固醇血症病因不明,临床上以血浆胆固醇浓度增高并在肌腱、皮下、角膜及血管内沉着为特征。胆固醇不溶于水,在血浆中以脂蛋白的形式运输.血浆中含量最多的低密度脂蛋白(LDL)是运输胆固醇的主要脂蛋白.因此,原发性高胆固醇血症表现为血浆LDL浓度的升高。血浆LDL是以极低密度脂蛋白(VLDL)     

膳食脂肪、碳水化合物、蛋白对血浆脂蛋白型别的影响

在等重条件下，膳食蛋白或个别氨基酸的不同类型一般对脂蛋白型别影响不大。膳食碳水化物取代脂肪时，有升高甘油三酯（TG）趋势，同时降低高密度脂蛋白（HDL）浓度，由于膳食纤维吸收速度不同，评估不同型别碳水化合物的不同效应有一定困难。饱和脂肪酸升高低密度脂蛋白（LDL）和HDL；而反式脂肪酸升高LDL而不升高HDL；不饱和脂肪酸降低LDL和HDL，多价不饱和脂肪酸甚于单价脂肪酸。     

玫瑰茄提取物对极低密度脂蛋白氧化修饰的作用

目的观察玫瑰茄提取物对Cu2+介导的极低密度脂蛋白(VLDL)氧化修饰的影响。方法采用一次性密度梯度离心法分离人血VLDL,用Cu2+进行体外氧化修饰,给药组在温育前加入一定浓度(终浓度:1.5 mg/ml)的玫瑰茄提取物,分别检测脂蛋白中丙二醛(MDA)及超氧化物歧化酶(SOD)的活性。结果玫瑰茄提取物可显著降低氧化型极低密度脂蛋白(ox-VLDL)中MDA的含量,明显提高脂蛋白中SOD活性。结论玫瑰茄提取物可显著抑制Cu2+诱导的VLDL氧化修饰。     

血脂正常患者颈动脉斑块与血脂、脂蛋白、载脂蛋白关系的研究

目的：研究血脂正常患者颈动脉斑块与血脂、脂蛋白、载脂蛋白的关系。方法：选择体检发现颈动脉粥样斑块者作为观察组,同期体检未见颈动脉斑块者作为对照组,并进一步分别根据斑块稳定性和血管狭窄程度将观察组分类,检测血液中甘油三酯（TG）、胆固醇（TC）、低密度脂蛋白（LDL）、高密度脂蛋白（HDL）、载脂蛋白A-Ⅰ（ApoA-Ⅰ）、载脂蛋白B（ApoB）。结果：观察组TC、TG水平与对照组差异无统计学意义（P〉0.05）,LDL、ApoB水平明显高于对照组,HDL、ApoA-Ⅰ水平明显低于对照组;斑块性质越硬、宫腔越狭窄,LDL、ApoB水平越高,HDL、ApoA-Ⅰ水平越低。结论：脂蛋白、载脂蛋白可以更敏感的反应颈动脉斑块的形成情况,LDL、ApoB水平升高、HDL、ApoA-Ⅰ水平降低与颈动脉斑块的形成密切相关。     

Plasma lipoprotein profile in fasted and refed chickens of two strains selected for high or low adiposity

The plasma lipoprotein profile has been determined in fasted and refed 5-week-old male broilers selected for low or high adiposity. Lipoprotein classes were subfractionated by density gradient ultracentrifugation, appearing as distinct bands with the following densities: very low density lipoprotein (VLDL), d less than 1.013 g/ml; low density lipoprotein (LDL), d 1.023-1.046 g/ml and high density lipoprotein (HDL), d 1.052-1.130 g/ml; the physiochemical characteristics (chemical composition, electrophoretic mobility and particle size) of these particles were then assessed. HDL, seen as a single band, represented 80% of total lipoproteins, with VLDL and LDL accounting for 1% and 16%, respectively, in fasted birds. Lipoprotein profiles were similar in fasted and refed animals of both lines, with the exception that VLDL levels were some 14-fold and 7-fold higher in the lean and fat lines, respectively, in the refed state. The VLDL of fasted birds of both lines were enriched in protein and relatively homogeneous in size; by contrast, VLDL in the refed state contained more triglyceride and less cholesteryl ester and protein and were larger and more heterogeneous, possibly representing a mixture of portomicrons and VLDL of hepatic origin. Birds of the fat line in both nutritional states differed from lean birds in exhibiting elevated plasma lipid and lipoprotein [VLDL, intermediate density lipoprotein (IDL) and HDL] levels, evidence that liver activity is directed toward increased lipoprotein production and secretion in that line.     

IDL,VLDL, chylomicrons and atherosclerosis

In humans with the lipoprotein lipase deficiency disorder large amounts of chylomicrons and large very low-density lipoprotein (VLDL) accumulate in plasma. In spite of this, atherosclerosis does not seem to develop at an accelerated rate, suggesting that these lipoproteins do not promote atherogenesis. In humans with dysbetalipoproteinemia remnant lipoproteins (intermediate density lipoprotein (IDL) plus B-VLDL) accumulate in plasma and these particles may therefore be the factor causing accelerated atherosclerosis in this disorder.Epidemiological studies in humans suggest that IDL or remnant lipoproteins are predictors of the severity or progression of atherosclerosis. Similar studies in the St. Thomas' Hospital rabbit strain, an animal model with genetically elevated plasma levels of VLDL, IDL and low-density lipoprotein (LDL), showed that IDL or remnant lipoproteins were better predictors of the extent of atherosclerosis than were LDL or VLDL.Studies of lipoprotein/arterial wall interactions have demonstrated that the larger the lipoprotein particle, the lower the influx into intima. Very large VLDL and chylomicrons do not seem to enter intima. Although high-density lipoprotein (HDL) enters intima faster than other lipoproteins, the small HDL particles seem to penetrate the entire arterial wall and leave via lymphatics and vasa vasorum in the outer media and adventitia. In contrast, LDL, and possibly also IDL and smaller VLDL, may only leave the intima via the lumen of the artery.In conclusion, a substantial body of evidence suggests that remnant lipoproteins (IDL and smaller VLDL) share with LDL the potential for promoting atherosclerosis, whereas very large VLDL and chylomicrons do not seem to have this effect.     

Effects of vitamin E deficiency on the distribution of cholesterol in plasma lipoproteins and the activity of cholesterol 7 alpha-hydroxylase in rabbit liver

Vitamin E-deficient rabbits with signs of muscular dystrophy showed accumulation of cholesterol in muscle as well as elevation of plasma cholesterol. The increase in plasma cholesterol was detected in low density lipoprotein (LDL) and very low density lipoprotein (VLDL) but not in high density lipoprotein (HDL) fractions of plasma lipoproteins. In liver, the activity of cholesterol 7 alpha-hydroxylase, the key enzyme involved in degradation of cholesterol, was approximately one-fifth that of control rabbits. Cytochrome P-450 level of liver microsomes was also reduced significantly. These results suggested that accumulation of cholesterol observed in dystrophic muscle of vitamin E-deficient rabbits may be due to an increase in LDL and VLDL cholesterol, the plasma lipoproteins carrying cholesterol to peripheral tissue, and to a decrease in cholesterol 7 alpha-hydroxylase activity, whose activity may have been affected by the reduced level of cytochrome P-450.     

Clustering and interrelationships of high-, low-, and very low-density lipoproteins in randomly recalled children and adults: The Cincinnati lipid research clinic's princeton school prevalence study

Within the frame of reference of no single, entirely satisfactory approach available for analysis of lipoprotein phenotypes, genotypes, and lipid—lipoprotein interactions with coronary heart disease, this analysis was designed to assess clustering of low-, high-, and very low-density lipoprotein cholesterols (LDL, HDL, and VLDL) in 943 randomly recalled children and 351 adults in the biracial Cincinnati Lipid Research Clinic's Princeton School Study using multivariate cluster analyses. The specific aims of this study were to better define and examine the interrelationships of LDL, HDL, and VLDL, and to focus upon the clinical and prognostic utility of multivariate cluster analysis of lipoproteins. The cluster analysis revealed a much more atherogenic constellation of lipoproteins for adults when compared with children, specifically, much higher adult LDL and VLDL with comparable HDL. Clusters of atherogenic and antiatherogenic lipoprotein cholesterols were substantively affected by race and sex. Whites were more likely to have predominantly elevated levels of LDL and/or VLDL with reciprocally low levels of HDL. Blacks, on the other hand, were more likely to have predominantly elevated HDL levels. White men primarily aggregated in clusters characterized by elevated LDL whereas white women aggregated in groups characterized by elevated HDL. Cluster analysis, a multidimensional scaling procedure, is a useful exploratory tool for assessment of the three-dimensional interactions of lipoprotein cholesterols and complements extant lipoprotein classification systems.     

Multivariate analysis of lipoprotein cholesterol fractions

Intervention and prevention of multifactorial diseases such as coronary heart disease can be effective only when the joint effects of multiple risk factors are known. This process is facilitated by multivariate analysis of correlated risk factors, such as the serum cholesterol fractions, high density lipoprotein (HDL), low density lipoprotein (LDL), and very low density lipoprotein (VLDL). Whereas evidence for genetic covariation provides focus for further refined biochemical analysis, covariation among environmental factors can point to efficacious intervention strategies. To assess sources of variation and covariation among HDL, LDL, and VLDL, a multivariate path model was developed and applied to family data. Phenotypic variance is due primarily to specific environmental influences with substantial genetic influences, with the common family environment contributing less than 10% of the variance. There are genetic correlations of -0.22 for HDL-VLDL and 0.35 for VLDL-LDL, consistent with the known inverse associations of HDL and VLDL and the precursor-product relationship between VLDL and LDL, whereas there is no evidence for a direct HDL-LDL genetic relationship. Strong specific environmental correlations are found between HDL and VLDL (-0.35 in children and -0.50 in adults). Thus, intervention focused primarily on one fraction (e.g., triglycerides and VLDL) might beneficially affect levels of both lipoproteins (e.g., lowering VLDL cholesterol and elevating HDL cholesterol). Multivariate analysis can facilitate understanding of the linked effects of intervention on lipoprotein cholesterols, and, hence, should benefit approaches to maximize the effects of lipoprotein cholesterol intervention on coronary heart disease morbidity and mortality.     

Apolipoprotein C-II modifications associated with an infusion of artificial lipid particles

Artificial lipid particles used as parenteral nutrition solution do not contain any apolipoproteins when they are infused into the circulation. Despite the absence of apolipoproteins, the metabolism of artificial lipid particles is similar to that of chylomicrons which contain various kinds of apolipoprotein. Of the known apolipoproteins, apolipoprotein C-II (apo C-II) is important in the hydrolysis of triglyceride-rich lipoproteins via involvement in the activation of lipoprotein lipase. Modifications of apo C-II associated with intravenous infusion of a lipid emulsion were investigated in eight patients. Changes in apo C-IIs in high density lipoproteins (HDL), low density lipoproteins (LDL) and very low density lipoproteins (VLDL) together with the plasma level of triglycerides, were quantified before and for 90 min after a bolus injection of a 10% lipid emulsion (1 ml/kg of body weight). Immediately prior to the injection, 54% of the total amount of apo C-II was present in HDL, while 27% was present in VLDL. After 5 to 10 min, the amount of apo C-II in HDL decreased to 29% of the total, while that in VLDL increased to 62%. Subsequently, the amounts of apo C-II in HDL and VLDL began to return to the preinjection levels. These variations in apo C-II were closely correlated with the plasma clearance of triglyceride. The result indicates that the injected lipids are not inert particles during their short intravascular life, but that they acquire apo C-II from HDL.     

Small supplements of N-3 fatty acids change serum low density lipoprotein composition by decreasing phospholipid and apolipoprotein B concentrations in young adult women

Summary In order to investigate the effect of a short-term application of marine n-3 polyunsaturated fatty acids on the composition of serum very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL), nine women aged 29±4.2 years, following a diet with a SFA/MUFA/PUFA profile of 2.4/3/1, received supplements of six capsules daily, each capsule containing 0.137 g of n-3 fatty acids (14.5% eicosapentaenoic acid (EPA) and 8.9% docosahexaenoic acid (DHA)) for 10 d. Food consumption, assessed during two 10-days periods indicates that percentage contribution of SFA, MUFA, and PUFA to the daily energy intake did not change through the fish-oil supplementation period, but the daily consumption of n-3 fatty acids increased 2.3 times. N-3 fatty supplementation increased EPA and DHA percentages in serum phospholipids, but failed to decrease (p>0.05) the cholesterol and triglyceride concentration in serum LDL and HDL, although it did so in VLDL. In contrast, the lipoprotein-phospholipid and lipoprotein-protein concentrations were markedly affected, mainly in LDL and HDL (at least p<0.01). HDL and VLDL compositions were not affected but the total mass (lipid+protein in mg/dl) concentration of these lipoproteins significantly decreased (p<0.05), suggesting a lower number of these particles in circulating blood after the n-3 treatment. The LDL-cholesterol/LDL-apolipoprotein B ratio increased (p<0.01) reflecting a probable increase in LDL size. Following fish oil supplementation, LDL particles contained a significantly lower amount of phospholipids, which also suggests changes in the surface/core ratio of the average LDL. Changes in serum lipoprotein lipids did not significantly correlate with any dietary change other than the n-3 fatty acid increase. The results indicate that a 10-day application of a small supplement of n-3 change the LDL composition leading to less atherogenic LDL particles with lower phospholipid and apolipoprotein (Apo) B concentrations. Received: 15 May 1998, Accepted: 28 August 1998     

Effects of dietary nucleotides upon lipoprotein pattern of newborn infants

Human milk differs widely from cow's milk in its nucleotide composition. This work examines the changes in the plasma lipoprotein pattern of 26 infants fed with human milk (HM), 35 with a milk formula (MF) and 23 with a nucleotide supplemented milk formula (NMF).Cholesterol increased in all infants from birth to one month of age. HM infants showed higher cholesterol concentrations than MF and NMF infants at one week of age but not at one month. High density lipoproteins (HDL) were increased in NMF infants compared to HM and MF infants at one week, and at 4 weeks after parturition. HDL were higher in infants fed HM and NMF than in those fed MF. Very low density lipoproteins (VLDL) increased in all groups of infants from birth until one month. At the latter age, HM and NMF infants showed considerably lower relative levels of VLDL than MF. Low-density lipoproteins (LDL) decreased in all newborns during the first month of life with no significant differences among the groups. Since the only difference between formulas was their relative content of acid soluble nucleotides, the HDL increase and VLDL decrease at one month of life in infants fed NMF compared to those fed MF may be ascribed to effects of dietary nucleotides on the lipoprotein metabolism during the neonatal period.     

Ⅱ型糖尿病患者膳食脂肪酸构成比推荐值研究

目的　阐明不同脂肪酸构成比对 型糖尿病患者餐后血脂代谢的影响 ,探索具有预防动脉粥样硬化作用的膳食脂肪酸构成比 (SFA∶ MUFA∶ PUFA)。方法　采用脂肪负荷餐后血脂代谢研究法 ,将 2 8例血糖控制稳定的 型糖尿病患者按两级分层抽样被随机地分为三组 ,禁食 1 2 h,分别接受脂肪酸构成比为 1∶ 1∶ 1 ( )、1∶ 1 .7∶ 1 .2 ( )和 1∶ 1 .7∶ 2 .3( )的脂肪负荷餐。测定餐前和餐后 2、4、6h血浆 TG、TC、HDL- C、Apo A1和 Apo B,LDL- C由公式计算得出。结果　各组餐后各时间点 TG较餐前明显升高 ,HDL- C和 Apo A1较餐前降低 , 、 和 组 TG峰时间 2～ 4、4和 4～ 6h,而 HDL- C和 Apo A1峰时间分别为 4、4和 6h;各组餐后 LDL- C和 Apo B较餐前降低 ,峰时间均在 4h。 组 LDL- C餐后 6h浓度和曲线下面积明显低于 和 组。多元逐步回归分析表明 ,MUFA/PUFA是影响餐后 2 h血浆总甘油三酯增值的因素 ,PUFA/SFA是影响LDL- C餐后曲线下面积的重要因素。结论　脂肪酸构成比不同可影响脂肪负荷餐后 型糖尿病患者血脂代谢动态 ; 组脂肪酸构成比可初步作为 型糖尿病患者膳食脂肪酸构成比的推荐值