载脂蛋白AI、AII、体重指数与血浆高密度脂蛋白亚类分布的关系
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摘要
Ⅰ.载脂蛋白AI水平与HDL亚类分布关系的研究
背景与目的：
载脂蛋白AI是高密度脂蛋白(HDL)中主要的蛋白质，它是细胞胆固醇逆向转运(RCT)的特殊重要因素。ApoAI能与磷脂，多种血浆因子及细胞膜受体结合，可以激活卵磷脂胆固醇酰基转移酶(LCAT)，起着促进细胞内胆固醇的移出，酯化，转移，以及调节HDL代谢的作用。本研究旨在探讨载脂蛋白水平主要是apoAI的水平对HDL亚类分布的影响。
方法：
采用双向电泳-免疫印迹检测法分析了545例受试者血浆HDL亚类的组成及含量。应用在受试人群呈正态分布的apoAI含量均值加或减一个标准差作为分割点将受试者分为3组即低apoAI组(apoAI≤1043．6mg/L)、中间apoAI组(1043．6＜apoAI＜1452．6mg/L)和高apoAI组(apoAI≥1452．6mg/L)。
结果：
1．与低apoAI水平组比较，中间及高apoAI水平组受试者所有HDL亚类的含量均逐渐显著的增加(p＜0．01～p＜0．001)。并且在高apoAI水平组，大颗粒的HDL_(2b)含量的增加较其小颗粒的preβ_1-HDL含量的增加更明显。
2．当apoAI及HDL-C水平同时升高时，高apoAI-HDL-C组较低apoAI-HDL-C组，其HDL_(2b)的含量增加116％，而preβ_1-HDL含量却仅仅增加了26％。
3．两两相关分析发现，apoAI水平与所有HDL亚类显著正相关，多元线性回归分析显示，apoAI水平为HDL亚类分布改变最有力的预测指标。
结论：
1．随血浆apoAI水平升高，所有HDL亚类，其含量都逐渐显著增加，尤其是大颗粒的HDL_(2b)最为明显。
2．当apoAI及HDL-C水平同时增加时，HDL向大颗粒转变更加明显。表明HDL成熟代谢过程加强，胆固醇逆向转运作用增强。
3．血浆apoAI水平是影响HDL亚类分布的的重要因素。
Ⅱ．血浆apoAⅡ含量对于HDL亚类分布的影响
背景与目的：
载脂蛋白AⅡ(apoAⅡ)是HDL颗粒中第二种主要的载脂蛋白，约占HDL中蛋白质总量的20％；apoAⅡ除了作为HDL的结构成份之外，还具有抑制卵磷脂胆固醇酯酰基转移酶(LCAT)及激活肝酯酶(HL)的作用。但是，ApoAⅡ与HDL亚类分布关系的研究却鲜有报道。本研究探讨血浆apoAⅡ含量对HDL亚类分布的影响，并分析apoAⅠ、apoAⅡ含量同时增加时，HDL亚类组成、分布所发生的变化。
方法：
采用双向电泳-免疫印迹检测法分析了292例受试者血浆HDL亚类的组成及含量。应用在受试人群呈正态分布的apoAⅠ和或apoAⅡ含量均值加或减一个标准差作为分割点把受试者分为低apoAⅡ组(apoAⅡ≤232．4mg/L)、中间apoAⅡ组(232．4＜apoAⅡ＜331．2mg/L)、高apoAⅡ组(apoAⅡ≥331．2mg/L)以及低apoAⅠ-apoAⅡ组(apoAⅠ≤1024．2mg/L及apoAⅡ≤232．4mg/L)、中间apoAⅠ-apoAⅡ组(1024．2＜apoAⅠ＜1446．6mg/L及232．4＜apoAⅡ＜331．2mg/L)和高apoAⅠ-apoAⅡ组(apoAⅠ≥1446．6mg/L及apoAⅡ≥331．2mg/L)。
结果：
1．与低apoAⅡ组比较，高apoAⅡ组HDL_(3a)，HDL_(3b)，和HDL_(2b)的含量显著增加(p＜0．01，p＜0．01，p＜0．01)。
2．当apoAⅠ及apoAⅡ水平同时增加时，所有HDL亚类的含量均逐渐显著升高。并且，高apoAⅠ-apoAⅡ组受试者HDL_(2b)的含量较低apoAⅠ-apoAⅡ组增加115％，preβ_1-HDL的含量仅增加了39％，HDL_(2b)含量增加更为明显。
3．两两相关以及多元回归分析均显示，血浆apoAⅠ水平与所有HDL亚类呈显著正相关，然而血浆apoAⅡ水平则仅与HDL_3及HDL_2呈正相关。
结论：
1．血浆apoAⅡ含量增多不仅可以引起大颗粒的HDL_(2b)含量的增加，而且可以导致小颗粒的HDL_3积聚。提示apoAⅡ水平在HDL颗粒成熟代谢的过程中可能起着双重的作用。
2．当apoAⅠ及apoAⅡ水平同时升高时，大颗粒HDL_(2b)的含量增加更为明显，表明HDL成熟代谢近一步增强。
Ⅲ．肥胖患者血浆HDL亚类分布的研究
背景与目的：
肥胖者以血浆TG水平升高、HDL-C水平降低为特征，与AS和CHD的发生密切相关。研究发现新生缺脂的小颗粒preβ_1-HDL从外周摄取胆固醇并在各种血浆因子，如卵磷脂-胆固醇酰基转移酶(LCAT)、胆固醇酯转运蛋白(CETP)、磷脂转运蛋白(PLTP)等的参与下，按preβ_1-HDL→preβ_2-HDL→preβ_3-HDL→HDL_3→HDL_2递变过程成熟，逐步转变为富含胆固醇酯的HDL_2从而被运至肝脏进一步降解。因此，HDL亚类组成、含量及分布变化与RCT有密切关系。本研究分析肥胖患者血浆HDL亚类的分布特征，为阐明HDL亚类组成、分布与肥胖人群As及CHD的发生机制提供新的依据。
方法：
采用双向电泳-免疫印迹检测法分析了581例中国人群血浆HDL亚类组成及含量。依据中国肥胖问题工作组推荐的体重指数(BMI)的标准，将受试者分为超轻组(BMI＜18．5kg/m~2)，合适组(BMI18．5-24kg/m~2)，超重组(24＜BMI≤28kg/m~2)以及肥胖组(BMI＞28kg/m~2)共四组。
结果：
1．与体重合适者比较，肥胖患者TG、preβ_1-HDL含量显著升高(p＜0．01，p＜0．01)，而HDL-C、HDL_(2a)、HDL_(2b)含量显著降低(p＜0．01，p＜0．05，p＜0．01)。
2．随血清BMI的升高，preβ_1-HDL含量显著逐渐增加，而HDL_(2b)含量显著逐渐减少(p＜0．01，p＜0．01)。
3．HDL颗粒变小的趋势在超重及肥胖患者中随着TG水平的升高更加明显。
4．两两相关分析揭示，超重及肥胖患者血浆TG、BMI与preβ_1-HDL含量显著正相关(p＜0．01)，与HDL_(2b)含量显著负相关(p＜0．01)。
5．多元线性回归分析发现，TG含量与高水平的preβ_1-HDL呈独立正相关而，与低水平的HDL_(2b)呈独立负相关。
结论：
超重者及肥胖患者血浆HDL颗粒呈变小趋势，而且这种趋势随血浆TG、BMI特别是TG水平升高更加明显。提示超重者及肥胖患者血浆HDL成熟代谢过程受阻，胆固醇逆向转运作用减弱。
Part One Relationship between apolipoprotein concentrations and HDL subclasses distribution
Background: Alterations in plasma apolipoproteins levels can influence the composition, content, and distribution of plasma lipoproteins that affect the risk of atherosclerosis. This study assessed the relationship between plasma apolipoproteins levels, mainly apoAI, and HDL subclass distribution.
Methods: The contents of plasma HDL subclasses were determined by 2-dimensional gel electrophoresis coupled with immunodetection in 545 Chinese subjects. We make use of the apoAI mean plus or minus 1 SD, So, the subjects were further subdivided into low apoAI group (apoAI≤1043.6mg/L), middle apoAI(1043.6＜apoAI＜1452.6) and high apoAI(apoAI≥1452.6mg/L) respectively.
Results: Compared with low apoAI group, the contents of all HDL subclasses increased significantly both in middle and high apoAI group, and the contents of large-sized HDL_(2b) increased more significantly relative to those of small-sized preβ_1-HDL in high apoAI group. Meanwhile, when apoAI and HDL-C levels increased simultaneously, in comparison to low apoAI along with HDL-C concentration group, a significant increased (116%) was shown in HDL_(2b) but only a slight increase (26%) in preβ_1-HDL. In addition, Pearson correlation analysis revealed that apoAI levels were positively and significantly correlated with all HDL subclasses. Multiple liner regression presented the apoAI concentrations were the most powerful predictor for HDL subclasses distribution.
Conclusion: With the elevation of apoAI concentrations, the contents of all HDL subclasses increased successively and significantly, especially, an increased in large-sized HDL2b. Further, when apoAI and HDL-C concentrations increased simultaneously, the shift to larger HDL size was more obvious. Which, in turn, indicated that HDL maturation might be enhanced and, the reverse cholesterol transport might be strengthened along with apoAI levels might be a more powerful factor to influence the distribution of HDL subclasses.
Part Two The influence of apolipoproteinAII concentrations on HDL subclasses distribution
Background: To investigate the impact of plasma apoAⅡconcentrations on the alteration of HDL subclasses distribution. And the cooperative effect of apoAⅠand apoAⅡon it.
Methods: The contents of plasma HDL subclasses were quantities by two-dimensional gel electrophoresis associated with immunodetection in 292 Chinese subjects. These subjects were divided into low apoAII (apoAⅡ≤232.4mg/L), middle apoAⅡ(232.4＜apoAⅡ＜331.2mg/L), high apoAII (apoAⅡ≥331.2mg/L) groups, low apoAⅠ-AⅡlevels (apoAⅠ≤1024.2mg/L together with apoAⅡ≤232.4mg/L), middle apoAⅠ-AⅡlevels (1024.2＜apoAⅠ＜1446.6mg/L together with 232.4＜apoAⅡ＜331.2mg/L) and high apoAⅠ-AⅢevels(apoAⅠ≥1446.6mg/L together with apoAⅡ≥331.2mg/L)groups according to the mean plus or minus 1 SD of apoAⅡor apoAⅠlevels as two cut-points.
Results: compared to the low apoAⅡgroup, the contents of HDLaa, HDLab, and HDL2b increased strikingly in high apoAⅡgroup. Moreover, the contents of all HDL subclasses increased progressively and significantly when apoAⅠand apoAⅡlevels increased simultaneously, and in comparison to low apoAⅠ-AⅡlevels group, the contents of large-sized nOL2b (115%)increased more significantly than those of small-sized preβ_1-HDL (39%) in high apoAⅠ-AⅡlevels group. In addition, Pearson correlation along with multiple liner regression results revealed that apoAI was positively and significantly correlated with all HDL subclasses while apoAII only showed positive association with HDL_(3a), HDL_(3b) and HDL_(2b).
Conclusion: excess apoAⅡcan cause the accumulation of both large-sized HDL_(2b) and small-sized HDL_3. Which implied that apoAII play a double role in the HDL maturation metabolism. Meanwhile, large-sized HDL_(2b) increased significantly when apoAI and apoAⅡlevels elevated simultaneously.
Part Three Alterations of High Density Lipoprotein Subclasses in Obese Subjects
Background: To investigate the characteristics of lipid metabolism in obese subjects, with particular emphasis on the alteration of HDL subclass contents and distribution.
Methods: Apo-AⅠcontents of serum HDL subclasses were quantitated by two-dimensional gel electrophoresis in 581 Chinese individuals. According to the BMI which the Working Group on Obesity in China (W G O C) under the support of International life sciences focal point in China recommend criterion, the subjects were divided into four groups: underweight group(BMI＜18.5kg/m~2),desirable group (BMI18.5-24kg/m~2), overweight group (24＜BMI≤28kg/m~2) and obesity group (BMI＞28kg/m~2).
Results: Concentrations of triglyceride, apoA-Ⅰcontent of preβ_1-HDL were significantly higher (P＜0.01 and P＜0.01, respectively), but, the levels of HDL-C, apoA-Ⅰcontents of HDL_(2a), HDL_(2b) were significantly lower (P＜0.01, P＜0.05 and P＜0.01, respectively) in obesity subjects versus desirable subjects. Moreover, with the elevation of BMI, small-sized preβ_1-HDL increased gradually and significantly, while large-sized HDL_(2b) decreased gradually and significantly in population. Meanwhile, the variations of HDL subclasses distribution above mentioned were more obvious with the elevation of TG levels in obesity along with overweight subjects. Pearson correlation analysis revealed that BMI, TG were positively correlated with preβ_1-HDL but negatively correlated with HDL_(2b) and multiple regression analysis also showed that TG concentrations were associated independently and positively with high pre_(β_1)-HDL; while correlated independently and negatively with low HDL_(2b) in obesity along with overweight subjects.
Conclusions: The particle size of HDL shifted toward smaller size in obesity and overweight subjects. Of note, the shift was more obvious with the elevation of BMI, especially TG levels. Which, in turn, indicated that HDL maturation might be abnormal, and reverse cholesterol transport might be weakened.
背景与目的：
载脂蛋白AI是高密度脂蛋白(HDL)中主要的蛋白质，它是细胞胆固醇逆向转运(RCT)的特殊重要因素。ApoAI能与磷脂，多种血浆因子及细胞膜受体结合，可以激活卵磷脂胆固醇酰基转移酶(LCAT)，起着促进细胞内胆固醇的移出，酯化，转移，以及调节HDL代谢的作用。本研究旨在探讨载脂蛋白水平主要是apoAI的水平对HDL亚类分布的影响。
方法：
采用双向电泳-免疫印迹检测法分析了545例受试者血浆HDL亚类的组成及含量。应用在受试人群呈正态分布的apoAI含量均值加或减一个标准差作为分割点将受试者分为3组即低apoAI组(apoAI≤1043．6mg/L)、中间apoAI组(1043．6＜apoAI＜1452．6mg/L)和高apoAI组(apoAI≥1452．6mg/L)。
结果：
1．与低apoAI水平组比较，中间及高apoAI水平组受试者所有HDL亚类的含量均逐渐显著的增加(p＜0．01～p＜0．001)。并且在高apoAI水平组，大颗粒的HDL_(2b)含量的增加较其小颗粒的preβ_1-HDL含量的增加更明显。
2．当apoAI及HDL-C水平同时升高时，高apoAI-HDL-C组较低apoAI-HDL-C组，其HDL_(2b)的含量增加116％，而preβ_1-HDL含量却仅仅增加了26％。
3．两两相关分析发现，apoAI水平与所有HDL亚类显著正相关，多元线性回归分析显示，apoAI水平为HDL亚类分布改变最有力的预测指标。
结论：
1．随血浆apoAI水平升高，所有HDL亚类，其含量都逐渐显著增加，尤其是大颗粒的HDL_(2b)最为明显。
2．当apoAI及HDL-C水平同时增加时，HDL向大颗粒转变更加明显。表明HDL成熟代谢过程加强，胆固醇逆向转运作用增强。
3．血浆apoAI水平是影响HDL亚类分布的的重要因素。
Ⅱ．血浆apoAⅡ含量对于HDL亚类分布的影响
背景与目的：
载脂蛋白AⅡ(apoAⅡ)是HDL颗粒中第二种主要的载脂蛋白，约占HDL中蛋白质总量的20％；apoAⅡ除了作为HDL的结构成份之外，还具有抑制卵磷脂胆固醇酯酰基转移酶(LCAT)及激活肝酯酶(HL)的作用。但是，ApoAⅡ与HDL亚类分布关系的研究却鲜有报道。本研究探讨血浆apoAⅡ含量对HDL亚类分布的影响，并分析apoAⅠ、apoAⅡ含量同时增加时，HDL亚类组成、分布所发生的变化。
方法：
采用双向电泳-免疫印迹检测法分析了292例受试者血浆HDL亚类的组成及含量。应用在受试人群呈正态分布的apoAⅠ和或apoAⅡ含量均值加或减一个标准差作为分割点把受试者分为低apoAⅡ组(apoAⅡ≤232．4mg/L)、中间apoAⅡ组(232．4＜apoAⅡ＜331．2mg/L)、高apoAⅡ组(apoAⅡ≥331．2mg/L)以及低apoAⅠ-apoAⅡ组(apoAⅠ≤1024．2mg/L及apoAⅡ≤232．4mg/L)、中间apoAⅠ-apoAⅡ组(1024．2＜apoAⅠ＜1446．6mg/L及232．4＜apoAⅡ＜331．2mg/L)和高apoAⅠ-apoAⅡ组(apoAⅠ≥1446．6mg/L及apoAⅡ≥331．2mg/L)。
结果：
1．与低apoAⅡ组比较，高apoAⅡ组HDL_(3a)，HDL_(3b)，和HDL_(2b)的含量显著增加(p＜0．01，p＜0．01，p＜0．01)。
2．当apoAⅠ及apoAⅡ水平同时增加时，所有HDL亚类的含量均逐渐显著升高。并且，高apoAⅠ-apoAⅡ组受试者HDL_(2b)的含量较低apoAⅠ-apoAⅡ组增加115％，preβ_1-HDL的含量仅增加了39％，HDL_(2b)含量增加更为明显。
3．两两相关以及多元回归分析均显示，血浆apoAⅠ水平与所有HDL亚类呈显著正相关，然而血浆apoAⅡ水平则仅与HDL_3及HDL_2呈正相关。
结论：
1．血浆apoAⅡ含量增多不仅可以引起大颗粒的HDL_(2b)含量的增加，而且可以导致小颗粒的HDL_3积聚。提示apoAⅡ水平在HDL颗粒成熟代谢的过程中可能起着双重的作用。
2．当apoAⅠ及apoAⅡ水平同时升高时，大颗粒HDL_(2b)的含量增加更为明显，表明HDL成熟代谢近一步增强。
Ⅲ．肥胖患者血浆HDL亚类分布的研究
背景与目的：
肥胖者以血浆TG水平升高、HDL-C水平降低为特征，与AS和CHD的发生密切相关。研究发现新生缺脂的小颗粒preβ_1-HDL从外周摄取胆固醇并在各种血浆因子，如卵磷脂-胆固醇酰基转移酶(LCAT)、胆固醇酯转运蛋白(CETP)、磷脂转运蛋白(PLTP)等的参与下，按preβ_1-HDL→preβ_2-HDL→preβ_3-HDL→HDL_3→HDL_2递变过程成熟，逐步转变为富含胆固醇酯的HDL_2从而被运至肝脏进一步降解。因此，HDL亚类组成、含量及分布变化与RCT有密切关系。本研究分析肥胖患者血浆HDL亚类的分布特征，为阐明HDL亚类组成、分布与肥胖人群As及CHD的发生机制提供新的依据。
方法：
采用双向电泳-免疫印迹检测法分析了581例中国人群血浆HDL亚类组成及含量。依据中国肥胖问题工作组推荐的体重指数(BMI)的标准，将受试者分为超轻组(BMI＜18．5kg/m~2)，合适组(BMI18．5-24kg/m~2)，超重组(24＜BMI≤28kg/m~2)以及肥胖组(BMI＞28kg/m~2)共四组。
结果：
1．与体重合适者比较，肥胖患者TG、preβ_1-HDL含量显著升高(p＜0．01，p＜0．01)，而HDL-C、HDL_(2a)、HDL_(2b)含量显著降低(p＜0．01，p＜0．05，p＜0．01)。
2．随血清BMI的升高，preβ_1-HDL含量显著逐渐增加，而HDL_(2b)含量显著逐渐减少(p＜0．01，p＜0．01)。
3．HDL颗粒变小的趋势在超重及肥胖患者中随着TG水平的升高更加明显。
4．两两相关分析揭示，超重及肥胖患者血浆TG、BMI与preβ_1-HDL含量显著正相关(p＜0．01)，与HDL_(2b)含量显著负相关(p＜0．01)。
5．多元线性回归分析发现，TG含量与高水平的preβ_1-HDL呈独立正相关而，与低水平的HDL_(2b)呈独立负相关。
结论：
超重者及肥胖患者血浆HDL颗粒呈变小趋势，而且这种趋势随血浆TG、BMI特别是TG水平升高更加明显。提示超重者及肥胖患者血浆HDL成熟代谢过程受阻，胆固醇逆向转运作用减弱。
Part One Relationship between apolipoprotein concentrations and HDL subclasses distribution
Background: Alterations in plasma apolipoproteins levels can influence the composition, content, and distribution of plasma lipoproteins that affect the risk of atherosclerosis. This study assessed the relationship between plasma apolipoproteins levels, mainly apoAI, and HDL subclass distribution.
Methods: The contents of plasma HDL subclasses were determined by 2-dimensional gel electrophoresis coupled with immunodetection in 545 Chinese subjects. We make use of the apoAI mean plus or minus 1 SD, So, the subjects were further subdivided into low apoAI group (apoAI≤1043.6mg/L), middle apoAI(1043.6＜apoAI＜1452.6) and high apoAI(apoAI≥1452.6mg/L) respectively.
Results: Compared with low apoAI group, the contents of all HDL subclasses increased significantly both in middle and high apoAI group, and the contents of large-sized HDL_(2b) increased more significantly relative to those of small-sized preβ_1-HDL in high apoAI group. Meanwhile, when apoAI and HDL-C levels increased simultaneously, in comparison to low apoAI along with HDL-C concentration group, a significant increased (116%) was shown in HDL_(2b) but only a slight increase (26%) in preβ_1-HDL. In addition, Pearson correlation analysis revealed that apoAI levels were positively and significantly correlated with all HDL subclasses. Multiple liner regression presented the apoAI concentrations were the most powerful predictor for HDL subclasses distribution.
Conclusion: With the elevation of apoAI concentrations, the contents of all HDL subclasses increased successively and significantly, especially, an increased in large-sized HDL2b. Further, when apoAI and HDL-C concentrations increased simultaneously, the shift to larger HDL size was more obvious. Which, in turn, indicated that HDL maturation might be enhanced and, the reverse cholesterol transport might be strengthened along with apoAI levels might be a more powerful factor to influence the distribution of HDL subclasses.
Part Two The influence of apolipoproteinAII concentrations on HDL subclasses distribution
Background: To investigate the impact of plasma apoAⅡconcentrations on the alteration of HDL subclasses distribution. And the cooperative effect of apoAⅠand apoAⅡon it.
Methods: The contents of plasma HDL subclasses were quantities by two-dimensional gel electrophoresis associated with immunodetection in 292 Chinese subjects. These subjects were divided into low apoAII (apoAⅡ≤232.4mg/L), middle apoAⅡ(232.4＜apoAⅡ＜331.2mg/L), high apoAII (apoAⅡ≥331.2mg/L) groups, low apoAⅠ-AⅡlevels (apoAⅠ≤1024.2mg/L together with apoAⅡ≤232.4mg/L), middle apoAⅠ-AⅡlevels (1024.2＜apoAⅠ＜1446.6mg/L together with 232.4＜apoAⅡ＜331.2mg/L) and high apoAⅠ-AⅢevels(apoAⅠ≥1446.6mg/L together with apoAⅡ≥331.2mg/L)groups according to the mean plus or minus 1 SD of apoAⅡor apoAⅠlevels as two cut-points.
Results: compared to the low apoAⅡgroup, the contents of HDLaa, HDLab, and HDL2b increased strikingly in high apoAⅡgroup. Moreover, the contents of all HDL subclasses increased progressively and significantly when apoAⅠand apoAⅡlevels increased simultaneously, and in comparison to low apoAⅠ-AⅡlevels group, the contents of large-sized nOL2b (115%)increased more significantly than those of small-sized preβ_1-HDL (39%) in high apoAⅠ-AⅡlevels group. In addition, Pearson correlation along with multiple liner regression results revealed that apoAI was positively and significantly correlated with all HDL subclasses while apoAII only showed positive association with HDL_(3a), HDL_(3b) and HDL_(2b).
Conclusion: excess apoAⅡcan cause the accumulation of both large-sized HDL_(2b) and small-sized HDL_3. Which implied that apoAII play a double role in the HDL maturation metabolism. Meanwhile, large-sized HDL_(2b) increased significantly when apoAI and apoAⅡlevels elevated simultaneously.
Part Three Alterations of High Density Lipoprotein Subclasses in Obese Subjects
Background: To investigate the characteristics of lipid metabolism in obese subjects, with particular emphasis on the alteration of HDL subclass contents and distribution.
Methods: Apo-AⅠcontents of serum HDL subclasses were quantitated by two-dimensional gel electrophoresis in 581 Chinese individuals. According to the BMI which the Working Group on Obesity in China (W G O C) under the support of International life sciences focal point in China recommend criterion, the subjects were divided into four groups: underweight group(BMI＜18.5kg/m~2),desirable group (BMI18.5-24kg/m~2), overweight group (24＜BMI≤28kg/m~2) and obesity group (BMI＞28kg/m~2).
Results: Concentrations of triglyceride, apoA-Ⅰcontent of preβ_1-HDL were significantly higher (P＜0.01 and P＜0.01, respectively), but, the levels of HDL-C, apoA-Ⅰcontents of HDL_(2a), HDL_(2b) were significantly lower (P＜0.01, P＜0.05 and P＜0.01, respectively) in obesity subjects versus desirable subjects. Moreover, with the elevation of BMI, small-sized preβ_1-HDL increased gradually and significantly, while large-sized HDL_(2b) decreased gradually and significantly in population. Meanwhile, the variations of HDL subclasses distribution above mentioned were more obvious with the elevation of TG levels in obesity along with overweight subjects. Pearson correlation analysis revealed that BMI, TG were positively correlated with preβ_1-HDL but negatively correlated with HDL_(2b) and multiple regression analysis also showed that TG concentrations were associated independently and positively with high pre_(β_1)-HDL; while correlated independently and negatively with low HDL_(2b) in obesity along with overweight subjects.
Conclusions: The particle size of HDL shifted toward smaller size in obesity and overweight subjects. Of note, the shift was more obvious with the elevation of BMI, especially TG levels. Which, in turn, indicated that HDL maturation might be abnormal, and reverse cholesterol transport might be weakened.
引文
[1] Gordon T, Castelli WP, Hiortland MC, Kannel WB, Dawber TR. (1977) High density lipoprotein as a protective factor against coronary heart disease :Framingham study. Am J Med 62707-62714.
[2] Watkins LO, Neaton JD, Kuller L H. (1986) Racial differences in high density lipoprotein cholesterol and coronary heart disease incidence in the usual care group of the multiple risk factor intervention trial. AmJ Cardiol 57538-57545.
[3] Gordon DJ, Probstifield JL, Garrison RJ,Bangdiwala S,Tyroler HA. (1989) High density lipoprotein cholesterol and cardiovascular disease.Four prospective American studies. Circulation 798-815.
[4] Atger V, Giral P, Simon A, Cambillau M, Levenson, Gariepy J, Megnien JL,Moatti N. (1995)High-density lipoprotein subtractions as markers of early atherosclerosis. Am J Cardiol 75,127-131.
[5] Von Eckardstein A,Huang Y,Assmann G (1994)Physiological role and clinical relevance of high-density lipoprotein subclasses.Curr Opin Lipidol 15404-15416.
[6]Wu XW, Fu MD,Lin BW. (1999)Study on the immunodetection method of HDL subclasses in human serum.Chin J Arterioscler 7,253-255.
[7] Xu Y, Fu MD. (2003) Alterations of HDL subclasses in hyperlipidemia. Clinica Chimica Acta 332,95-102.
[8] Jonas A, Kezdy KE, Wald JH. (1989)Defined apolipoprotein A-I conformations in reconstituted high density lipoprotein discs. J Biol Chem 264,4818-4824.
[9] Rye K-A Clay MA, Barter PJ. (1999) Remodelling of high density lipoproteins by plasma factors. Atherosclerosis 145,227-238.
[10] Kwiterovich Jr PO. (1998)The antiatherogenic role of high-density lipoprotein cholesterol.Am J Cardiol 82,13Q-21Q.
[11] Yuye,Yang, Bingyu Yan, Mingde Fu, Yanhua Xu,Ying Tian. (2005)Relationship between plasma lipid concentrations and HDL subclasses. Clinica Chimica Acta 354,49-58.
[12] Lantu Gou, Mingde Fu, Yanhua Xu, Ying Tian, Bingyu Yan, Luchuan Yang. (2005) Alteraions of HDL subclasses in endogenous hypertriglyceridemia. Am Heart J 150,1039-1045.
[13] Lianqun Jia,Shiyin Long,Mingde Fu,Bingyu Yan.Ying Tian,Yanhua Xu,Lantu Gou. (2006)Relationship between total cholesterol/high-density lipoprotein cholesterol ratio,triglyceride/high-density lipoprotein cholesterol ratio,and high-density lipoprotein subclasses.Metabolism Clinical and Experimental (in press).
[14] Li Tian, Lianqun Jia, Mingde Fu,Ying Tian, Yanhua Xu, Haoming Tian, Yuye Yang.(2006)Alterations of High Density Lipoprotein Subclasses in Obese Subjects. Lipids 41,789-796.
[15] Executive summary of the third report of NCEP, (2001) expert panel on detection, evaluation and treatment of high blood cholesterol in adults. Adult Treatment Panel III. JAMA 285,486-497.
[16] Warnick GR, Nguyen T, Albers AA. (1985)Comparison of improved precipitation methods for quantification of high-density lipoprotein cholesterol.Clin Chem 31,217-222.
[17] Friedwald WF, Levy RI, Fredrickson DS: (1972) Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Cheml8,499-502.
[18] Labeur C, Shepherd J, Rosseneu M. (1990) Immunological assays of apolipoproteins in plasma:methods and instrumentation.Clin Chem 36,591-597.
[19] Liu B. (1995)Immunoassay of human plasma apolipoproteins and clinical applications.In:Wang KQ,editor.Lipoproteins and atherosclerosis.Beijing: People' s Health Press; 359-368.
[20] Gordon D, Rifking BM. (1989) Current concepts:high density lipoproteins-the clinical implications of recent studies.N Engl J Med 321,1311-1315.
[21] Hirano K, Yamashita S. (1995)Atherosclerotic disease in marked hyperalphalipoproteinemiaxombined reduction of cholesteryl ester transfer protein and hepatic triglyceride lipase. Arterioscler Thromb Vasc Biol. 15,1849-1856.
[22] Berard AM, Foger B. (1997)High plasma HDL concentrations associated with enhanced atherosclerosis in transgenic mice overexpressing lecithin-cholesteryl acyltransferase. Nat Med. 3,744-749.
[23] Hoeg JM, Santamarina-Fojo S. (1996) Overexpression of lecithin:cholesterol acyltransferase in transgenic rabbits prevents diet-induced atherosclerosis. Proc Nat Acad Sci USA. 93,11448-11453.
[24] Arnold Von Eckardstein (2001) High density lipoproteins and Arteriosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology. 21,13.
[25] Edward M, Rubin Y, Ishida, Shirley M, Clift, Ronald M, Kranss. (1991) Expression of human apolipoprotein A-I in transgenic mice results in reduced plasma levels of murine apolipoprotein A-I and the appearance of two new high density lipoprotein size subclasses. Biochemistry 88,434-438.
[26] Kunitake STm Ka La Sala KJ, Kane JP. (1985) ApolipoproteinA-I-containing lipoproteins with pre-beta electrophoretic mobility. J Lipid Res 26,549-555.
[27] Asztalos BF,Sloop CH,Wong L. (1993)Two-dimensional electrophoresis of plasma lipoproteins:recognition of new apo A-I-containing subpopulations.Biochim Biophys Acta 1169,291-300.
[28] Castro GR,Fielding CJ. (1988)Early incorporation of cell derived cholesterol into preβ-migrating high-density lipoprotein.Biochemistry 27,:25-29.
[29] Miida T, Kawano M, Fielding CJ. (1992) Regulation of the concentration of preβ high-density lipoprotein in normal plasma by cell membranes and lecithinxholesterol acyltransferase activity. Biochemistry 31,11112-11117.
[30] Miida T, Yamaguchi T, Tsuda T, Okada M(1998).High prebetal-HDL levels in hypercholesterolemia are maintained by probucol but reduced by a low-cholesterlo diet.Atherosclerosis. 138,128-134.
[1] Paigen, U. Mitchell, D. Reue, K. Morrow, A, Lusis, A. J. and LeBoeuf, R. Ath-I, a gene determining atherosclerosis susceptibility and high density lipoprotein. Proc Notl Acad Sci U S A 1987; 84:3763-3767.
[2] Miller, G. J. and Miller, N. E. High density lipoprotein concentration and development of ischemic heart disease. Lancet 1975; 1:16-19.
[3] Schaefer. E. J. Heaton. W. H. Wetzel. M. G. and Brewer. H. B. plasma apolipoproteinAI absence associated with a marked reduction of high density lipoproteins and premature coronary artery disease. Atherosclerosis 1982; 2:16-26.
[4] Miller N. E. Hammett, F. Saltissi, S. Rao, S. van Zeller, H., Coultart, J. and Lewis, B. Relation of angiographically defined coronary artery disease to plasma lipoprotein subfractions and apolipoproteins. Br Med J 1981; 282:1741-1744.
[5] Noma, A., Yokosuka, T. and Kitamura, K. Plasma lipids and apolipoproteins as discriminators for presence and severity of angiographically defined coronary artery disease. Atherosclerosis 1983; 37:157-162.
[6] Miller, N. E. Associations of high-density lipoprotein subclasses and apolipoproteins with ischemic heart disease and atherosclerosis. Am Heart J 1987; 113: 589-597.
[7] Gordon, D. J. and Rifiind, B. M. High-density lipoprotein the clinical implications of recent studies. New Engl J Med 1989; 321:1311-1316.
[8]Von Eckardstein A, Huang Y, Assmann G. Physiological role and clinical relevance of high-density lipoprotein subclasses. Curr Opin Lipidol 1994; 5:404-416.
[9]XuY, FuM. Alterations of HDL subclasses in hyperlipidemia. Clin Chim Acta 2003; 332:95-102.
[10] Yang YY, Yan BY,Fu MD,Xu YH,Tian Y. Relationship between plasma lipid concentrations and HDL subclasses. Clin Chim Acta 2005;354:49-58.
[11] Wu X, Fu M, Liu B. Study on the immunodetection method of HDL subclasses in human plasma. Chin J Areterioscler 1999;7:253-255.
[12] Cheung MC,Brown BG,Wolf AC. Altered particle size distribution of apoA-I-containing HDL subpopulations in patients with coronary heart disease. J Lipid Res 1991; 32:383-394.
[13] Asztalos BF,Cupples LA,Demissie S,et al. High-density lipoprotein subpopulation profile and coronary heart disease prevalence in male participants of the Framingham Offspring Study. Arterioscler Thromb Vasc Biol 2004;24:2181-2187.
[14] Dobiasova M, Frohlich J. Understanding the mechanism of LCAT reaction may help to explain the high predictive value of LDL/HDL cholesterol ratio. Physiol Res 1998; 47:387-397.
[15] Lantu Gou, Mingde Fu, Yanhua Xu, Ying Tian, Bingyu Yan, Luchuan Yang. Alterations of HDL subclasses in endogenous hypertriglyceridemia. Am Heart J 2005; 150:1039-1045.
[16] Lianqun Jia,Shiyin Long,Mingde Fu,Bingyu Yan,Ying Tian,Yanhua Xu,Lantu Gou. Relationship between total cholesterol/high-density lipoprotein cholesterol ratio,triglyceride/high-density lipoprotein cholesterol ratio, and high-density lipoprotein subclasses. Metabolism Clinical and Experimental 2006;55:1141-1148.
[17] Tall, A. Plasma high density lipoproteins. Metabolism and relationship to atherogenesis. J Clin Invest 1990; 86: 379-384.
[18] Liu B. Immunoassay of human plasma apolipoproteins and clinical applications. In: Wang kQ, editor. Lipoproteins and Atherosclerosis. Beijing: People's Health Press; 1995; p.359-68.
[19]Asztalos BF,Collins D, Cupples A. Value if high-density lipoprotein(HDL)subpopulations in predicting recurrent cardiovascular events in the veterans affairs HDL Intervention Trial. Arterioscler Thromb Vasc Biol 2005;25:2185-2191.
[20]Asztalos BF,Horvath KV,McNamara JR, Roheim PS,Rubinstein JJ,Schaefer EJ. Comparing the effects of five different statins on the HDL subpopulation profiles of coronary heart disease patients. Atherosclerosis 2002; 164:361-369.
[21] Asztalos BF,Demissie S,Cupples LA,. LpA-I,LpA-I:A-II HDL and CHD-risk:The Framingham Offspring Study and the Veterans Affaires HDL Intervention Trial. Atherosclerosis 2005;November 17
[22] Genest JJ Jr, Martin-Munley SS, McNamara JR, et al. Familial lipoprotein disorders in patients with premature coronary artery disease. Circulation 1992;85:2025-2031.
[23] Barber PJ, Rye, KA. High density lipoprotein cholesterol and coronary heart disease. Atherosclerosis 1996;121:1-6.
[24] Lagocki, P. A. & Scanu, A. M.In vitro modulation of the apolipoprotein composition of high density lipoprotein.Displacement of apolipoproteinAI from high density lipoprotein by apolipoproteinA-II. J Biol Chem 1980;255: 3701-3706.
[25] Warden CH, Hedrick CC, Qiao JH, Castellani LW, Lusis AJ. Atherosclerosis in transgenic mice overexpressing apolipoprotein A-II. Science 1993;261:469-472.
[26] Mehrabian M, Qiao J-H, Hyman R, Ruddle D, Laughton, Lusis AJ.Influence of the apoA-II gene locus on HDL levels and fatty streak development in mice. Arterioscler Thromb 1993;13:1-10.
[27] Escola-Gil JC, Marzal-Casacuberta A, Julve-Gil J, Ishida BY, Ordonez-Llanos J, Chan L, Gonzalez-Sastre F, Blanco-Vaca F.Human apolipoproteinA-II is a pro-atherogenic molecule when it is expressed in transgenic mice at a level similar to that in humans: evidence of a potentially relevant species-specific interaction with diet. J Lipid Resl998;39:457-462.
[28] Schultz, J. R., E. L. Gong, M. R. McCall, A. V. Nichols, S. M. Clift, and E. M. Rubin. Expression of human apolipoprotein A-II and its effect on high density lipoproteins in transgenic mice. J Biol Chem 1992; 267: 21630-21636.
[29] Deeb, S. S., Cheung, M. C, Peng, R., Wolf, A. C, Stern, R., Albers, J. J. And knopp ,R.H. A mutation in the human apolipoproteinA-I gene.Dominant effect on the level and characteristics of plasma high density lipoproteins. J Biol Chem 1991;266:13654-13660.
[30] Edward M, Rubin Y, Ishida, Shirley M, Clift, Ronald M, Kranss. Expression of human apolipoprotein A-I in transgenic mice results in reduced plasma levels of murine apolipoprotein A-I and the appearance of two new high density lipoprotein size subclasses. Biochemistry 1991;88:434-438.
[31]Kunitake STm Ka La Sala KJ, Kane JP.ApolipoproteinA-I-containing lipoproteins with pre-beta electrophoretic mobility. J Lipid Res 1985;26:549-555.
[32] Asztalos BF, Sloop CH,Wong L. Two-dimensional electrophoresis of plasma lipoproteins:recognition of new apo A-I-containing subpopulations. Biochim Biophys Acta 1993;1169:291-300.
[33]Saidi Y, Sich D, Camproux A,. Interrelationships between postprandial lipoprotein B.CIII particle changes and high-density lipoprotein subclass profiles in mixed hyperlipoproteinemia. Metabolism 1999;48:60-67.
[34] Catherine C. Hedrick, Lawrence W. Castedllani, Howard Wong, Aldons J. Lusis. In vivo interactions of apoA-Ⅱ, apoA-Ⅰ, and hepatic lipase contribution to HDL structure and antiatherogenic functions. J Lipid Res 2001; 42(4): 563-570.
[1] Gordon T, Castelli WP, Hiortland MC, et al. (1977) Density lipoprotein as a protective factor against coronary heart disease: Framingham study. Am J Med 62,707-714.
[2] Gordon DJ, Probstfield JL, Garrison RJ, et al. (1989) High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. Circulation 79,8-15.
[3] Wilson PWF, Agostino RB, Levy D, et al. (1998) Prediction of coronary heart disease using risk factor categories. Circulation 97,1837-1847.
[4] Goldbourt U, Yaari S, Medalie JH. (1997) Isolated low HDL cholesterol as a risk factor for coronary heart disease mortality: a 21-year follow-up of 8000 men. Arterioscler Thromb Vasc Biol 17,107-113.
[5] Fielding CJ, Fielding PE.(1995) Molecular physiology of reverse cholesterol transport. J Lipid Res 36,211-228.
[6] Cheung MC, Brown BG, Wolf AC. (1991) Altered particle size distribution of apoAI-containing HDL subpopulations in patients with coronary heart disease. Arterioscler Thromb Vasc Biol 32,383-394.
[7] Atger V, Giral P, Simon A, Cambillan M, et al. (1995) High-density lipoprotein subfractions as markers of early atherosclerosis. Am J Cardiol 75,127-131.
[8] Von Eckardstein A, Huang Y, Assmann G (1994) Physiological role and clinical relevance of high-density lipoprotein subclasses. Curr Opin Lipidol 5,404-416.
[9] Patsch W, Schonfeld G, Gotto AM Jr, et al. (1980) Characterization of human high density by zonal ultracentrifugation. J Biol Chem 255,3178-3185.
[10] Chung BH, Wilkinson T, Geer JC, et al. (1980) Preparative and quantitative isolation of plasma lipoproteins: rapid single discontinuous density gradient ultracentrifugation in vertical rotor. J Lipid Res 21,284-291.
[11] Albers JJ, Warnick GR, Wiebe D, et al. (1978) Multi-Laboratory comparison of three heparin-Mn~(2+) precipitation procedures for estimating cholesterol in high density lipoprotein. Clin Chem 24,853-856.
[12] Soedamah-Muthu SS, Colhoun HM, Thomason MJ, et al. (2003) The effect of atorvastatin on serum lipids, lipoproteins and NMR spectroscopy defined lipoprotein subclasses in type 2 diabetic patients with ischaemic heart disease. Atherosclerosis 167,243-255.
[13] Williams PT, Krauss RM, Nichols AY, et al. (1990) Identifying the predominant peak diameter of high-density and low-density lipoproteins by electrophoresis. Lipid Res 31,1131-1139.
[14] Wu XW, Fu MD, Liu BW. (1999) Study on the immunodetection method of HDL subclasses in human serum. Chin J Arterioscler 7,253-255.
[15] Xu YH, Fu MD.(2003) Alterations of HDL subclasses in hyperlipidemia. Clinica Chimica Acta 332,95-102.
[16] Johansson J, Carlson LA, Landou C, et al. (1991) High density lipoproteins and coronary atherosclerosis. A strong inverse relation with the largest particles confined to normotriglyceridemic patients. Arterioscler Thormb 11,174-182.
[17] Barbaras R, Puchois P, Fruchart JC, Aihand G. (1987) Cholesterol efflux from cultured adipose cells is mediated by Lp-AI particles but not by LpAI:AII particles. Biochem Biophys Res Commun 142,63-69.
[18] Hubert HB, Feinleib M, McNamara PM, et al.(1983) Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up on participants in the Framingham Heart Study. Circulation.67,968-977.
[19] Bertiere MC, Fumerun F, Rigand D, et al. (1998) Low high density lipoprotein-2 Concentrations in obese male subjects. Atherosclerosis 73,57-61.
[20] Jean-Pie(?)e Despres,Isabelle Lemieax,Gilles-R,et al. (2000) HDL-cholesterol as a marker of coronary heart disease risk: the Quebec cardiovascular study. Atherosclerosis 153,263-272.
[21] Assmann G, Schulte H. (1992) Relation of high-density cholesterol and triglycerides to incidence of atherosclerotic coronary artery disease (the PROCAM experience). Am J Cardiol 70,733-737.
[22] Hokanson JE, Austin MA. (1996)Plasma triglyceride is a risk factor for cardiovascular disease independent of high density lipoprotein cholesterol: a meta analyses of population based prospective studies. J Cardiovasc Risk 3,213-219.
[23] Cooperative Meta-analysis Group of China Task Force (2002): Predictive values of body mass index and waist circumference to risk factors of related diseases in Chinese adult population. Chin J Epidemiol 23,5-10.
[24] Executive Summary of the Third Report of NCEP (2001), Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults. Adult Treatment Panel III. JAMA 285,486-497.
[25] Kissebah AH, Peiris AN. (1989) Biology of regional body fat distribution: relationship to NIDDM. Diabetes Metab Rev 5,83-109.
[26] Kissebah AH, Freedman DS, Peiris AN. (1989) Health risks of obesity. Med Clin N Am 73,111-138.
[27] Despres JP, Moorjani S, Lupien PJ, et al. (1990) Regional distribution of body fat, plasma lipoproteins, and cardiovascular disease. Arteriosclerosis 10,497-511.
[28] Despres JP. (1991)Obesity and lipid metabolism: relevance of body fat distribution. Curr Opin Lipidol 2,5-15.
[29] Gou LT, Fu MD, Xu YH, et al. (2005) Alterations of HDL subclasses in endogenous hypertriglyceridemia. Am Heart J 150,1039-1045.
[30] Yang YY, Yan BY, Fu MD, et al. (2005) Relationship between plasma lipid concentrations and HDL subclasses. Clin Chim Acta 354,49-58.
[31] Jia LQ, Bai H, Fu MD, et al. (2005) Relationship between plasma HDL subclasses distribution and apoA-I gene polymorphisms. Clin Chim Acta 360,37-45.
[32] Long SY, Tian Y, Fu MD, et al. Relationship between plasma HDL subclasses distribution and lipoprotein lipase gene Hind III polymorphism in hyperlipidemia. Clin Chim Acta 366,316-321.
[33] Rye KA, Clay MA, Barter PJ. (1999) Remodeling of high density lipoproteins by plasma factors. Atherosclerosis 145, 227-238.
[34] Saidi Y, Sich D, Camproux A, et al.(1999) Interrelationships between postprandial lipoprotein B: CⅢ particles changes and high-density lipoprotein subclass profiles in mixed hyperlipoproteinemia. Metabolism 48, 60-67.
[35] Barrans A, Collet X, Barbaras R, et al.(1994) Hepatic lipase induces the formation of pre-β-1-high density lipoprotein(HDL) from triacylglycerol-rich HDL_2. J Biol Chem 269, 11572-11577.
[36] Miida T, Yamaguchi T, Tsuda T, et al.(1998) High prebetal-HDL levels in hypercholesterolemia are maintained by probucol but reduced by a low-cholesterol diet. Atherosclerosis 138, 129-134.
[37] Lee M, Kim JQ, Kim J, et al.(2001) Studies on the plasma lipid profiles, and LCAT and CETP activities according to hypedipoproteinemia phenotypes(HLP). Atherosclerosis 159, 381-389.
[38] Alberts JJ, Pitman W, Wolfabauer G, et al.(1999) Relationship between phospholipid transfer protein activity and HDL level and size amonginbred mouse strains. J Lipid Res 40(2), 295-297.
[39] Grundy, S. M. and G. L Vega.(1992) Two different views of the relationship of hypertriglyceridemia to coronary heart disease. implications for treatment. Arch Intern Med 152, 28-34.
[1] Brouillette CG, Anantharamaiah GM. Structural models of human apolipoprotein A-I. Biochem Biophys Acta 1995; 1256: 103-129.
[2] Segrest JP, Li L, Anantharamaiah GM, et al. Structure and function of apolipoprotein A-I and high-density lipoprotein. Curr Opin Lipidol 2000; 11: 105-115.
[3] Li Tian, Mingde Fu, Lianqun Jia, Yanhua Xu, et al. Relationship between apolipoprotein concentrations and HDL subclasses distribution. Lipids(2007, in press).
[4] Assmann, G, G. Schmitz, H. Funke, and A. von Eckardstein. Apolipoprotein A-I and HDL deficiency. Curr. Opin. Lipidol 1990; 1: 110-115.
[5] SomaM. R. Donetti E. Parolini C. Calabresi L. Recombinant apolipoproteinA-I_(MILANO) dimer inhibits carotid intimal thickening in hypercholesterolemic rabbits. Atherosclerosis 1994; 109: 321.
[6] Shah P. K. Nilsson J. Kaul S. Fishbein M. C. Effects of recombinant apolipoproteinAI(Milano)on aortic atherosclerosis in apolipoprotein E-deficient mice. Circulation 1998; 97: 780-785.
[7] Li D. Weng S. Yang B. Inhibition of arterial thrombus formation by apoAI Milano. Arterioscler Thromb Vasc Biol 1999; 19: 378-383.
[8] Ordovas JM, Cassidy DK, Civeira K, Bisgaier CL, Schaefer EJ. Familial apolipoprotein A-Ⅰ, C-Ⅲ, and A-Ⅳ deficiency and premature atherosclerosis due to deletion of a gene complex on chromosome 11. J Biol Chem 1989; 264: 16339-16345.
[9] Karathanasis SK, Ferris E, Haddad IA. DNA inversion within the apolipoproteins AI/CIII/AIV-encoding gene cluster of certain patients with premature atherosclerosis. Proc Natl Acad Sci U S A 1987;87:7198-7203.
[10] Williamson R, Lee D, Hagaman J. Marked reduction of high density lipoprotein cholesterol in mice genetically modified to lack apolipoprotein A-I. Proc Natl Acad Sci USA 1992;89:7134-7138.
[11] Walsh A,Ito Y,Breslow JL.High levels of human apolipoproteinAI in transgenic mice result in increased plasma levels of small high density lipoprotein(HDL)particles comparable to human HDL, J Biol Chem 1989;264:6488-6494.
[12] Rubin EM.Krauss RM, Spangler EA,Verstuyft JG,Clift SM.Inhibition of early atherogenesis in transgenic mice by human apolipoproteinAI. Nature 1991;19:265-267.
[13] Swanson ME, Hughes TE,Denny IS et al.High level expression of human apolipoproteinAI in transgenic rats raises total serum high density lipoprotein cholesterol and lowers rat apolipoproteinAI. Transgenic Res 1992;1:142-147.
[14] Deeb S.S.Takata K.Peng R.Kajiyama G A splice-junction mutation responsible for familial apolipoproteinAII deficiency. Am J Human Genet 1990;46:822-827.
[15] Hedric CC.Castellani LW.Warden CH. Influence of mouse apolipoprotein A-II on plasma lipoproteins in transgenic miceBiol Chem 1993;268:20676-20682.
[16] Ikewaki K.Zech L.A.Kindt M.ApolipoproteinAII production rate is a major factor regulating the distribution of apolipoproteinAI among HDL subclasses LpA-I and LpA-I:AII in normolipidemic humans. Arterioscler Thromb Vasc Biol 1995;15:306-312.
[17] Mowri H.Patsch JR..ApolipoproteinAII influences the substrate properties of human HDL2 and HDL3 for hepatic lipase. Arterioscler Thromb Vasc Biol 1996;16:755.
[18] Zhong S.Goldberg L.Human apoAII inhibits the hydrolysis of HDL triglyceride and the decrease of HDL size induced by hypertriglyceridemia and cholesteryl ester transfer protein in transgenic mice. J Clin Invest 1994;94:2457-2467.
[19] Lagrost L,Persegol L,Lallemant C.Influence of apolipoprotein particles on cholesteryl ester transfer protein activity. Particles containing varilus proportions of apolipoproteinAI and AII.Biol Chem 1994;269:3189-3197.
[20] Li Tian,Mingde Fu, Lianqun Jia, et al.The influence of apolipoproteinAII concentrations on HDL subclasses distribution.
[21] Duverger N,Viglietta C,Berthou L et al.Transgenic rabbits expressing human apolipoproteinAI in the liver. Arterioscler Thromb Vasc Biol 1996;16:1424-1429.
[22] Paszty C, Maeda N,Verstuyft J,Rubin EM.ApolipoproteinAI transgene corrects apolipoprotein E deficiency-induced atherosclerosis in mice. J Clin Invest 1994;94:899-903.
[23] Schultz JR, Gong EL, McCall MR,Nichols AV,Clift SM.Expression of human apolipoproteinAII and its effect on high density lipoproteins in transgenic mice.J Biol Chem 1992;267:21630-21636.
[24] McCombs R.J.Mercadis D.E.Ellis J.Attenuated hypercholesterolemic response to a high-cholesterol diet in subjects heterozygous for the apolipoproteinAIV-2 allele.N.Engl.J.Med.1994;331:706-710.
[25] Von Eckardstein A.Huang Y.Wu S.Sarmandi A.S.Lipoproteins containing apolipoproteinAIV but not apolipoprotein AI take up and esterify cell-derived cholesterol in plasma. Arterioscler Thromb Vasc Biol 1995;15:1755-1763.
[26] Duverger N.Tremp G.Caillaud J.Protection against atherosclerosis in mice mediated by human apolipoproteinAIV.Science 1996;273:966-968.
[27] Goldberg I.J.Scheraldi C.A.Yaxoub L.K.Saxena U.Lipoprotein lipase:modulation by apoAIV.J.Biol Chem. 1990;265:4266-4272.
[28] Wai-man R. Wong, Emma Hawe, Lai K. Li, George J. Miller, Viviane Nicaud. Apolipoprotein AIV Gene Variant S347 Is Associated With Increased Risk of Coronary Heart Disease and Lower Plasma Apolipoprotein AIV Levels. Circulation Research 2003;92:969.
[2] Watkins LO, Neaton JD, Kuller L H. (1986) Racial differences in high density lipoprotein cholesterol and coronary heart disease incidence in the usual care group of the multiple risk factor intervention trial. AmJ Cardiol 57538-57545.
[3] Gordon DJ, Probstifield JL, Garrison RJ,Bangdiwala S,Tyroler HA. (1989) High density lipoprotein cholesterol and cardiovascular disease.Four prospective American studies. Circulation 798-815.
[4] Atger V, Giral P, Simon A, Cambillau M, Levenson, Gariepy J, Megnien JL,Moatti N. (1995)High-density lipoprotein subtractions as markers of early atherosclerosis. Am J Cardiol 75,127-131.
[5] Von Eckardstein A,Huang Y,Assmann G (1994)Physiological role and clinical relevance of high-density lipoprotein subclasses.Curr Opin Lipidol 15404-15416.
[6]Wu XW, Fu MD,Lin BW. (1999)Study on the immunodetection method of HDL subclasses in human serum.Chin J Arterioscler 7,253-255.
[7] Xu Y, Fu MD. (2003) Alterations of HDL subclasses in hyperlipidemia. Clinica Chimica Acta 332,95-102.
[8] Jonas A, Kezdy KE, Wald JH. (1989)Defined apolipoprotein A-I conformations in reconstituted high density lipoprotein discs. J Biol Chem 264,4818-4824.
[9] Rye K-A Clay MA, Barter PJ. (1999) Remodelling of high density lipoproteins by plasma factors. Atherosclerosis 145,227-238.
[10] Kwiterovich Jr PO. (1998)The antiatherogenic role of high-density lipoprotein cholesterol.Am J Cardiol 82,13Q-21Q.
[11] Yuye,Yang, Bingyu Yan, Mingde Fu, Yanhua Xu,Ying Tian. (2005)Relationship between plasma lipid concentrations and HDL subclasses. Clinica Chimica Acta 354,49-58.
[12] Lantu Gou, Mingde Fu, Yanhua Xu, Ying Tian, Bingyu Yan, Luchuan Yang. (2005) Alteraions of HDL subclasses in endogenous hypertriglyceridemia. Am Heart J 150,1039-1045.
[13] Lianqun Jia,Shiyin Long,Mingde Fu,Bingyu Yan.Ying Tian,Yanhua Xu,Lantu Gou. (2006)Relationship between total cholesterol/high-density lipoprotein cholesterol ratio,triglyceride/high-density lipoprotein cholesterol ratio,and high-density lipoprotein subclasses.Metabolism Clinical and Experimental (in press).
[14] Li Tian, Lianqun Jia, Mingde Fu,Ying Tian, Yanhua Xu, Haoming Tian, Yuye Yang.(2006)Alterations of High Density Lipoprotein Subclasses in Obese Subjects. Lipids 41,789-796.
[15] Executive summary of the third report of NCEP, (2001) expert panel on detection, evaluation and treatment of high blood cholesterol in adults. Adult Treatment Panel III. JAMA 285,486-497.
[16] Warnick GR, Nguyen T, Albers AA. (1985)Comparison of improved precipitation methods for quantification of high-density lipoprotein cholesterol.Clin Chem 31,217-222.
[17] Friedwald WF, Levy RI, Fredrickson DS: (1972) Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Cheml8,499-502.
[18] Labeur C, Shepherd J, Rosseneu M. (1990) Immunological assays of apolipoproteins in plasma:methods and instrumentation.Clin Chem 36,591-597.
[19] Liu B. (1995)Immunoassay of human plasma apolipoproteins and clinical applications.In:Wang KQ,editor.Lipoproteins and atherosclerosis.Beijing: People' s Health Press; 359-368.
[20] Gordon D, Rifking BM. (1989) Current concepts:high density lipoproteins-the clinical implications of recent studies.N Engl J Med 321,1311-1315.
[21] Hirano K, Yamashita S. (1995)Atherosclerotic disease in marked hyperalphalipoproteinemiaxombined reduction of cholesteryl ester transfer protein and hepatic triglyceride lipase. Arterioscler Thromb Vasc Biol. 15,1849-1856.
[22] Berard AM, Foger B. (1997)High plasma HDL concentrations associated with enhanced atherosclerosis in transgenic mice overexpressing lecithin-cholesteryl acyltransferase. Nat Med. 3,744-749.
[23] Hoeg JM, Santamarina-Fojo S. (1996) Overexpression of lecithin:cholesterol acyltransferase in transgenic rabbits prevents diet-induced atherosclerosis. Proc Nat Acad Sci USA. 93,11448-11453.
[24] Arnold Von Eckardstein (2001) High density lipoproteins and Arteriosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology. 21,13.
[25] Edward M, Rubin Y, Ishida, Shirley M, Clift, Ronald M, Kranss. (1991) Expression of human apolipoprotein A-I in transgenic mice results in reduced plasma levels of murine apolipoprotein A-I and the appearance of two new high density lipoprotein size subclasses. Biochemistry 88,434-438.
[26] Kunitake STm Ka La Sala KJ, Kane JP. (1985) ApolipoproteinA-I-containing lipoproteins with pre-beta electrophoretic mobility. J Lipid Res 26,549-555.
[27] Asztalos BF,Sloop CH,Wong L. (1993)Two-dimensional electrophoresis of plasma lipoproteins:recognition of new apo A-I-containing subpopulations.Biochim Biophys Acta 1169,291-300.
[28] Castro GR,Fielding CJ. (1988)Early incorporation of cell derived cholesterol into preβ-migrating high-density lipoprotein.Biochemistry 27,:25-29.
[29] Miida T, Kawano M, Fielding CJ. (1992) Regulation of the concentration of preβ high-density lipoprotein in normal plasma by cell membranes and lecithinxholesterol acyltransferase activity. Biochemistry 31,11112-11117.
[30] Miida T, Yamaguchi T, Tsuda T, Okada M(1998).High prebetal-HDL levels in hypercholesterolemia are maintained by probucol but reduced by a low-cholesterlo diet.Atherosclerosis. 138,128-134.
[1] Paigen, U. Mitchell, D. Reue, K. Morrow, A, Lusis, A. J. and LeBoeuf, R. Ath-I, a gene determining atherosclerosis susceptibility and high density lipoprotein. Proc Notl Acad Sci U S A 1987; 84:3763-3767.
[2] Miller, G. J. and Miller, N. E. High density lipoprotein concentration and development of ischemic heart disease. Lancet 1975; 1:16-19.
[3] Schaefer. E. J. Heaton. W. H. Wetzel. M. G. and Brewer. H. B. plasma apolipoproteinAI absence associated with a marked reduction of high density lipoproteins and premature coronary artery disease. Atherosclerosis 1982; 2:16-26.
[4] Miller N. E. Hammett, F. Saltissi, S. Rao, S. van Zeller, H., Coultart, J. and Lewis, B. Relation of angiographically defined coronary artery disease to plasma lipoprotein subfractions and apolipoproteins. Br Med J 1981; 282:1741-1744.
[5] Noma, A., Yokosuka, T. and Kitamura, K. Plasma lipids and apolipoproteins as discriminators for presence and severity of angiographically defined coronary artery disease. Atherosclerosis 1983; 37:157-162.
[6] Miller, N. E. Associations of high-density lipoprotein subclasses and apolipoproteins with ischemic heart disease and atherosclerosis. Am Heart J 1987; 113: 589-597.
[7] Gordon, D. J. and Rifiind, B. M. High-density lipoprotein the clinical implications of recent studies. New Engl J Med 1989; 321:1311-1316.
[8]Von Eckardstein A, Huang Y, Assmann G. Physiological role and clinical relevance of high-density lipoprotein subclasses. Curr Opin Lipidol 1994; 5:404-416.
[9]XuY, FuM. Alterations of HDL subclasses in hyperlipidemia. Clin Chim Acta 2003; 332:95-102.
[10] Yang YY, Yan BY,Fu MD,Xu YH,Tian Y. Relationship between plasma lipid concentrations and HDL subclasses. Clin Chim Acta 2005;354:49-58.
[11] Wu X, Fu M, Liu B. Study on the immunodetection method of HDL subclasses in human plasma. Chin J Areterioscler 1999;7:253-255.
[12] Cheung MC,Brown BG,Wolf AC. Altered particle size distribution of apoA-I-containing HDL subpopulations in patients with coronary heart disease. J Lipid Res 1991; 32:383-394.
[13] Asztalos BF,Cupples LA,Demissie S,et al. High-density lipoprotein subpopulation profile and coronary heart disease prevalence in male participants of the Framingham Offspring Study. Arterioscler Thromb Vasc Biol 2004;24:2181-2187.
[14] Dobiasova M, Frohlich J. Understanding the mechanism of LCAT reaction may help to explain the high predictive value of LDL/HDL cholesterol ratio. Physiol Res 1998; 47:387-397.
[15] Lantu Gou, Mingde Fu, Yanhua Xu, Ying Tian, Bingyu Yan, Luchuan Yang. Alterations of HDL subclasses in endogenous hypertriglyceridemia. Am Heart J 2005; 150:1039-1045.
[16] Lianqun Jia,Shiyin Long,Mingde Fu,Bingyu Yan,Ying Tian,Yanhua Xu,Lantu Gou. Relationship between total cholesterol/high-density lipoprotein cholesterol ratio,triglyceride/high-density lipoprotein cholesterol ratio, and high-density lipoprotein subclasses. Metabolism Clinical and Experimental 2006;55:1141-1148.
[17] Tall, A. Plasma high density lipoproteins. Metabolism and relationship to atherogenesis. J Clin Invest 1990; 86: 379-384.
[18] Liu B. Immunoassay of human plasma apolipoproteins and clinical applications. In: Wang kQ, editor. Lipoproteins and Atherosclerosis. Beijing: People's Health Press; 1995; p.359-68.
[19]Asztalos BF,Collins D, Cupples A. Value if high-density lipoprotein(HDL)subpopulations in predicting recurrent cardiovascular events in the veterans affairs HDL Intervention Trial. Arterioscler Thromb Vasc Biol 2005;25:2185-2191.
[20]Asztalos BF,Horvath KV,McNamara JR, Roheim PS,Rubinstein JJ,Schaefer EJ. Comparing the effects of five different statins on the HDL subpopulation profiles of coronary heart disease patients. Atherosclerosis 2002; 164:361-369.
[21] Asztalos BF,Demissie S,Cupples LA,. LpA-I,LpA-I:A-II HDL and CHD-risk:The Framingham Offspring Study and the Veterans Affaires HDL Intervention Trial. Atherosclerosis 2005;November 17
[22] Genest JJ Jr, Martin-Munley SS, McNamara JR, et al. Familial lipoprotein disorders in patients with premature coronary artery disease. Circulation 1992;85:2025-2031.
[23] Barber PJ, Rye, KA. High density lipoprotein cholesterol and coronary heart disease. Atherosclerosis 1996;121:1-6.
[24] Lagocki, P. A. & Scanu, A. M.In vitro modulation of the apolipoprotein composition of high density lipoprotein.Displacement of apolipoproteinAI from high density lipoprotein by apolipoproteinA-II. J Biol Chem 1980;255: 3701-3706.
[25] Warden CH, Hedrick CC, Qiao JH, Castellani LW, Lusis AJ. Atherosclerosis in transgenic mice overexpressing apolipoprotein A-II. Science 1993;261:469-472.
[26] Mehrabian M, Qiao J-H, Hyman R, Ruddle D, Laughton, Lusis AJ.Influence of the apoA-II gene locus on HDL levels and fatty streak development in mice. Arterioscler Thromb 1993;13:1-10.
[27] Escola-Gil JC, Marzal-Casacuberta A, Julve-Gil J, Ishida BY, Ordonez-Llanos J, Chan L, Gonzalez-Sastre F, Blanco-Vaca F.Human apolipoproteinA-II is a pro-atherogenic molecule when it is expressed in transgenic mice at a level similar to that in humans: evidence of a potentially relevant species-specific interaction with diet. J Lipid Resl998;39:457-462.
[28] Schultz, J. R., E. L. Gong, M. R. McCall, A. V. Nichols, S. M. Clift, and E. M. Rubin. Expression of human apolipoprotein A-II and its effect on high density lipoproteins in transgenic mice. J Biol Chem 1992; 267: 21630-21636.
[29] Deeb, S. S., Cheung, M. C, Peng, R., Wolf, A. C, Stern, R., Albers, J. J. And knopp ,R.H. A mutation in the human apolipoproteinA-I gene.Dominant effect on the level and characteristics of plasma high density lipoproteins. J Biol Chem 1991;266:13654-13660.
[30] Edward M, Rubin Y, Ishida, Shirley M, Clift, Ronald M, Kranss. Expression of human apolipoprotein A-I in transgenic mice results in reduced plasma levels of murine apolipoprotein A-I and the appearance of two new high density lipoprotein size subclasses. Biochemistry 1991;88:434-438.
[31]Kunitake STm Ka La Sala KJ, Kane JP.ApolipoproteinA-I-containing lipoproteins with pre-beta electrophoretic mobility. J Lipid Res 1985;26:549-555.
[32] Asztalos BF, Sloop CH,Wong L. Two-dimensional electrophoresis of plasma lipoproteins:recognition of new apo A-I-containing subpopulations. Biochim Biophys Acta 1993;1169:291-300.
[33]Saidi Y, Sich D, Camproux A,. Interrelationships between postprandial lipoprotein B.CIII particle changes and high-density lipoprotein subclass profiles in mixed hyperlipoproteinemia. Metabolism 1999;48:60-67.
[34] Catherine C. Hedrick, Lawrence W. Castedllani, Howard Wong, Aldons J. Lusis. In vivo interactions of apoA-Ⅱ, apoA-Ⅰ, and hepatic lipase contribution to HDL structure and antiatherogenic functions. J Lipid Res 2001; 42(4): 563-570.
[1] Gordon T, Castelli WP, Hiortland MC, et al. (1977) Density lipoprotein as a protective factor against coronary heart disease: Framingham study. Am J Med 62,707-714.
[2] Gordon DJ, Probstfield JL, Garrison RJ, et al. (1989) High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. Circulation 79,8-15.
[3] Wilson PWF, Agostino RB, Levy D, et al. (1998) Prediction of coronary heart disease using risk factor categories. Circulation 97,1837-1847.
[4] Goldbourt U, Yaari S, Medalie JH. (1997) Isolated low HDL cholesterol as a risk factor for coronary heart disease mortality: a 21-year follow-up of 8000 men. Arterioscler Thromb Vasc Biol 17,107-113.
[5] Fielding CJ, Fielding PE.(1995) Molecular physiology of reverse cholesterol transport. J Lipid Res 36,211-228.
[6] Cheung MC, Brown BG, Wolf AC. (1991) Altered particle size distribution of apoAI-containing HDL subpopulations in patients with coronary heart disease. Arterioscler Thromb Vasc Biol 32,383-394.
[7] Atger V, Giral P, Simon A, Cambillan M, et al. (1995) High-density lipoprotein subfractions as markers of early atherosclerosis. Am J Cardiol 75,127-131.
[8] Von Eckardstein A, Huang Y, Assmann G (1994) Physiological role and clinical relevance of high-density lipoprotein subclasses. Curr Opin Lipidol 5,404-416.
[9] Patsch W, Schonfeld G, Gotto AM Jr, et al. (1980) Characterization of human high density by zonal ultracentrifugation. J Biol Chem 255,3178-3185.
[10] Chung BH, Wilkinson T, Geer JC, et al. (1980) Preparative and quantitative isolation of plasma lipoproteins: rapid single discontinuous density gradient ultracentrifugation in vertical rotor. J Lipid Res 21,284-291.
[11] Albers JJ, Warnick GR, Wiebe D, et al. (1978) Multi-Laboratory comparison of three heparin-Mn~(2+) precipitation procedures for estimating cholesterol in high density lipoprotein. Clin Chem 24,853-856.
[12] Soedamah-Muthu SS, Colhoun HM, Thomason MJ, et al. (2003) The effect of atorvastatin on serum lipids, lipoproteins and NMR spectroscopy defined lipoprotein subclasses in type 2 diabetic patients with ischaemic heart disease. Atherosclerosis 167,243-255.
[13] Williams PT, Krauss RM, Nichols AY, et al. (1990) Identifying the predominant peak diameter of high-density and low-density lipoproteins by electrophoresis. Lipid Res 31,1131-1139.
[14] Wu XW, Fu MD, Liu BW. (1999) Study on the immunodetection method of HDL subclasses in human serum. Chin J Arterioscler 7,253-255.
[15] Xu YH, Fu MD.(2003) Alterations of HDL subclasses in hyperlipidemia. Clinica Chimica Acta 332,95-102.
[16] Johansson J, Carlson LA, Landou C, et al. (1991) High density lipoproteins and coronary atherosclerosis. A strong inverse relation with the largest particles confined to normotriglyceridemic patients. Arterioscler Thormb 11,174-182.
[17] Barbaras R, Puchois P, Fruchart JC, Aihand G. (1987) Cholesterol efflux from cultured adipose cells is mediated by Lp-AI particles but not by LpAI:AII particles. Biochem Biophys Res Commun 142,63-69.
[18] Hubert HB, Feinleib M, McNamara PM, et al.(1983) Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up on participants in the Framingham Heart Study. Circulation.67,968-977.
[19] Bertiere MC, Fumerun F, Rigand D, et al. (1998) Low high density lipoprotein-2 Concentrations in obese male subjects. Atherosclerosis 73,57-61.
[20] Jean-Pie(?)e Despres,Isabelle Lemieax,Gilles-R,et al. (2000) HDL-cholesterol as a marker of coronary heart disease risk: the Quebec cardiovascular study. Atherosclerosis 153,263-272.
[21] Assmann G, Schulte H. (1992) Relation of high-density cholesterol and triglycerides to incidence of atherosclerotic coronary artery disease (the PROCAM experience). Am J Cardiol 70,733-737.
[22] Hokanson JE, Austin MA. (1996)Plasma triglyceride is a risk factor for cardiovascular disease independent of high density lipoprotein cholesterol: a meta analyses of population based prospective studies. J Cardiovasc Risk 3,213-219.
[23] Cooperative Meta-analysis Group of China Task Force (2002): Predictive values of body mass index and waist circumference to risk factors of related diseases in Chinese adult population. Chin J Epidemiol 23,5-10.
[24] Executive Summary of the Third Report of NCEP (2001), Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults. Adult Treatment Panel III. JAMA 285,486-497.
[25] Kissebah AH, Peiris AN. (1989) Biology of regional body fat distribution: relationship to NIDDM. Diabetes Metab Rev 5,83-109.
[26] Kissebah AH, Freedman DS, Peiris AN. (1989) Health risks of obesity. Med Clin N Am 73,111-138.
[27] Despres JP, Moorjani S, Lupien PJ, et al. (1990) Regional distribution of body fat, plasma lipoproteins, and cardiovascular disease. Arteriosclerosis 10,497-511.
[28] Despres JP. (1991)Obesity and lipid metabolism: relevance of body fat distribution. Curr Opin Lipidol 2,5-15.
[29] Gou LT, Fu MD, Xu YH, et al. (2005) Alterations of HDL subclasses in endogenous hypertriglyceridemia. Am Heart J 150,1039-1045.
[30] Yang YY, Yan BY, Fu MD, et al. (2005) Relationship between plasma lipid concentrations and HDL subclasses. Clin Chim Acta 354,49-58.
[31] Jia LQ, Bai H, Fu MD, et al. (2005) Relationship between plasma HDL subclasses distribution and apoA-I gene polymorphisms. Clin Chim Acta 360,37-45.
[32] Long SY, Tian Y, Fu MD, et al. Relationship between plasma HDL subclasses distribution and lipoprotein lipase gene Hind III polymorphism in hyperlipidemia. Clin Chim Acta 366,316-321.
[33] Rye KA, Clay MA, Barter PJ. (1999) Remodeling of high density lipoproteins by plasma factors. Atherosclerosis 145, 227-238.
[34] Saidi Y, Sich D, Camproux A, et al.(1999) Interrelationships between postprandial lipoprotein B: CⅢ particles changes and high-density lipoprotein subclass profiles in mixed hyperlipoproteinemia. Metabolism 48, 60-67.
[35] Barrans A, Collet X, Barbaras R, et al.(1994) Hepatic lipase induces the formation of pre-β-1-high density lipoprotein(HDL) from triacylglycerol-rich HDL_2. J Biol Chem 269, 11572-11577.
[36] Miida T, Yamaguchi T, Tsuda T, et al.(1998) High prebetal-HDL levels in hypercholesterolemia are maintained by probucol but reduced by a low-cholesterol diet. Atherosclerosis 138, 129-134.
[37] Lee M, Kim JQ, Kim J, et al.(2001) Studies on the plasma lipid profiles, and LCAT and CETP activities according to hypedipoproteinemia phenotypes(HLP). Atherosclerosis 159, 381-389.
[38] Alberts JJ, Pitman W, Wolfabauer G, et al.(1999) Relationship between phospholipid transfer protein activity and HDL level and size amonginbred mouse strains. J Lipid Res 40(2), 295-297.
[39] Grundy, S. M. and G. L Vega.(1992) Two different views of the relationship of hypertriglyceridemia to coronary heart disease. implications for treatment. Arch Intern Med 152, 28-34.
[1] Brouillette CG, Anantharamaiah GM. Structural models of human apolipoprotein A-I. Biochem Biophys Acta 1995; 1256: 103-129.
[2] Segrest JP, Li L, Anantharamaiah GM, et al. Structure and function of apolipoprotein A-I and high-density lipoprotein. Curr Opin Lipidol 2000; 11: 105-115.
[3] Li Tian, Mingde Fu, Lianqun Jia, Yanhua Xu, et al. Relationship between apolipoprotein concentrations and HDL subclasses distribution. Lipids(2007, in press).
[4] Assmann, G, G. Schmitz, H. Funke, and A. von Eckardstein. Apolipoprotein A-I and HDL deficiency. Curr. Opin. Lipidol 1990; 1: 110-115.
[5] SomaM. R. Donetti E. Parolini C. Calabresi L. Recombinant apolipoproteinA-I_(MILANO) dimer inhibits carotid intimal thickening in hypercholesterolemic rabbits. Atherosclerosis 1994; 109: 321.
[6] Shah P. K. Nilsson J. Kaul S. Fishbein M. C. Effects of recombinant apolipoproteinAI(Milano)on aortic atherosclerosis in apolipoprotein E-deficient mice. Circulation 1998; 97: 780-785.
[7] Li D. Weng S. Yang B. Inhibition of arterial thrombus formation by apoAI Milano. Arterioscler Thromb Vasc Biol 1999; 19: 378-383.
[8] Ordovas JM, Cassidy DK, Civeira K, Bisgaier CL, Schaefer EJ. Familial apolipoprotein A-Ⅰ, C-Ⅲ, and A-Ⅳ deficiency and premature atherosclerosis due to deletion of a gene complex on chromosome 11. J Biol Chem 1989; 264: 16339-16345.
[9] Karathanasis SK, Ferris E, Haddad IA. DNA inversion within the apolipoproteins AI/CIII/AIV-encoding gene cluster of certain patients with premature atherosclerosis. Proc Natl Acad Sci U S A 1987;87:7198-7203.
[10] Williamson R, Lee D, Hagaman J. Marked reduction of high density lipoprotein cholesterol in mice genetically modified to lack apolipoprotein A-I. Proc Natl Acad Sci USA 1992;89:7134-7138.
[11] Walsh A,Ito Y,Breslow JL.High levels of human apolipoproteinAI in transgenic mice result in increased plasma levels of small high density lipoprotein(HDL)particles comparable to human HDL, J Biol Chem 1989;264:6488-6494.
[12] Rubin EM.Krauss RM, Spangler EA,Verstuyft JG,Clift SM.Inhibition of early atherogenesis in transgenic mice by human apolipoproteinAI. Nature 1991;19:265-267.
[13] Swanson ME, Hughes TE,Denny IS et al.High level expression of human apolipoproteinAI in transgenic rats raises total serum high density lipoprotein cholesterol and lowers rat apolipoproteinAI. Transgenic Res 1992;1:142-147.
[14] Deeb S.S.Takata K.Peng R.Kajiyama G A splice-junction mutation responsible for familial apolipoproteinAII deficiency. Am J Human Genet 1990;46:822-827.
[15] Hedric CC.Castellani LW.Warden CH. Influence of mouse apolipoprotein A-II on plasma lipoproteins in transgenic miceBiol Chem 1993;268:20676-20682.
[16] Ikewaki K.Zech L.A.Kindt M.ApolipoproteinAII production rate is a major factor regulating the distribution of apolipoproteinAI among HDL subclasses LpA-I and LpA-I:AII in normolipidemic humans. Arterioscler Thromb Vasc Biol 1995;15:306-312.
[17] Mowri H.Patsch JR..ApolipoproteinAII influences the substrate properties of human HDL2 and HDL3 for hepatic lipase. Arterioscler Thromb Vasc Biol 1996;16:755.
[18] Zhong S.Goldberg L.Human apoAII inhibits the hydrolysis of HDL triglyceride and the decrease of HDL size induced by hypertriglyceridemia and cholesteryl ester transfer protein in transgenic mice. J Clin Invest 1994;94:2457-2467.
[19] Lagrost L,Persegol L,Lallemant C.Influence of apolipoprotein particles on cholesteryl ester transfer protein activity. Particles containing varilus proportions of apolipoproteinAI and AII.Biol Chem 1994;269:3189-3197.
[20] Li Tian,Mingde Fu, Lianqun Jia, et al.The influence of apolipoproteinAII concentrations on HDL subclasses distribution.
[21] Duverger N,Viglietta C,Berthou L et al.Transgenic rabbits expressing human apolipoproteinAI in the liver. Arterioscler Thromb Vasc Biol 1996;16:1424-1429.
[22] Paszty C, Maeda N,Verstuyft J,Rubin EM.ApolipoproteinAI transgene corrects apolipoprotein E deficiency-induced atherosclerosis in mice. J Clin Invest 1994;94:899-903.
[23] Schultz JR, Gong EL, McCall MR,Nichols AV,Clift SM.Expression of human apolipoproteinAII and its effect on high density lipoproteins in transgenic mice.J Biol Chem 1992;267:21630-21636.
[24] McCombs R.J.Mercadis D.E.Ellis J.Attenuated hypercholesterolemic response to a high-cholesterol diet in subjects heterozygous for the apolipoproteinAIV-2 allele.N.Engl.J.Med.1994;331:706-710.
[25] Von Eckardstein A.Huang Y.Wu S.Sarmandi A.S.Lipoproteins containing apolipoproteinAIV but not apolipoprotein AI take up and esterify cell-derived cholesterol in plasma. Arterioscler Thromb Vasc Biol 1995;15:1755-1763.
[26] Duverger N.Tremp G.Caillaud J.Protection against atherosclerosis in mice mediated by human apolipoproteinAIV.Science 1996;273:966-968.
[27] Goldberg I.J.Scheraldi C.A.Yaxoub L.K.Saxena U.Lipoprotein lipase:modulation by apoAIV.J.Biol Chem. 1990;265:4266-4272.
[28] Wai-man R. Wong, Emma Hawe, Lai K. Li, George J. Miller, Viviane Nicaud. Apolipoprotein AIV Gene Variant S347 Is Associated With Increased Risk of Coronary Heart Disease and Lower Plasma Apolipoprotein AIV Levels. Circulation Research 2003;92:969.
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