Insulin resistance and adiposity influence lipoprotein size and subclass concentrations. Results from the Insulin Resistance Atherosclerosis Study
Insulin resistance and adiposity influence lipoprotein size and subclass concentrations. Results from the Insulin Resistance Atherosclerosis Study
复制标题
DOI：
10.1016/j.metabol.2004.09.002
复制
发表时间：
2005-02-01
影响因子：
9.8
通讯作者：
Otvos, JD
中科院分区：
文献类型：
--
作者：
Goff, DC;D'Agostino, RB;Otvos, JD
背景：胰岛素抵抗和肥胖与血脂异常有关，血脂异常包括高水平的甘油三酯（TG）、低水平的高密度脂蛋白胆固醇（HDL-C）和低密度脂蛋白胆固醇（LDL-C）水平无变化。我们检查了胰岛素抵抗和肥胖与脂蛋白颗粒大小、浓度和亚类浓度的关系。方法：胰岛素抵抗动脉粥样硬化研究是一项针对中年男性和女性的多中心队列研究。使用标准方法测定脂蛋白脂质浓度。使用核磁共振技术测定脂蛋白大小、颗粒浓度和亚类浓度。胰岛素抵抗（S-1）是根据频繁采样的静脉内葡萄糖耐量试验和MINMOD程序确定的。 S-1 越高代表胰岛素抵抗越低。评估了空腹胰岛素、体重指数、腰围和腰臀比。 结果：1371 名参与者中，女性 754 名，男性 617 名； 459 名西班牙裔、383 名非裔美国人和 529 名非西班牙裔白人； 437 名患有 2 型糖尿病，301 名患有糖耐量受损，633 名患有正常糖耐量。平均（SD）年龄为55.5（8.5）岁，体重指数为29.3（5.8）kg/m（2），S-1为1.6（1.8）单位。根据年龄、性别和种族进行调整后，S 与 LDL-C 无关 (r = 0.01)；然而，S 与 LDL 大小 (r = 0.34，P < .001)、LDL 颗粒浓度 (r = -0.28，P < .001)、小 LDL (r = -0.3，P < .001)、中 LDL (r = -0.37，P < .001) 和大 LDL (r = 0.21，P < .001) 相关。此外，S 与 TG (r = -0.36，P < .001)、VLDL 颗粒 (r = -0.08，P < .01)、大 VLDL (r = -0.32，P < .001)、VLDL 大小 (r = -0.38，P < .001)、HDL-C (r = 0.37，P < .001)、HDL 颗粒 (r = 0.09，P < .001），大 HDL（r = 0.31，P < .001）和 HDL 大小（r = 0.33，P < .001）。因子分析揭示了一个因子占脂蛋白测量值方差的 41.4%，并且与 S 相关（r = -0.33，P < .001）。对于空腹胰岛素和肥胖的脂蛋白测量分析，也观察到了类似的相反方向的结果。结论：与胰岛素抵抗和肥胖相关的血脂异常包括对脂蛋白代谢的影响，而在传统的脂蛋白胆固醇和总甘油三酯检查时，这些影响被忽略了。在研究胰岛素抵抗和肥胖在动脉粥样硬化的发病机制和预防中的作用时，应检查脂蛋白的大小和亚类。 (C) 2005 Elsevier Inc. 保留所有权利。
Background: Insulin resistance and obesity are associated with a dyslipidemia composed of high levels of triglycerides (TG), low levels of high-density lipoprotein cholesterol (HDL-C), and no change in level of low-density lipoprotein cholesterol (LDL-C). We examined the association of insulin resistance and adiposity with lipoprotein particle size, concentration, and subclass concentrations.Methods: The Insulin Resistance Atherosclerosis Study is a multicenter cohort study of middle-aged men and women. Lipoprotein lipid concentrations were determined using standard methods. Lipoprotein size, particle concentration, and subclass concentrations were determined using nuclear magnetic resonance technology. Insulin resistance (S-1) was determined based on the frequently sampled intravenous glucose tolerance test and the MINMOD program. A higher S-1 represents less insulin resistance. Fasting insulin, body mass index, waist circumference, and waist/hip ratio were assessed.Results: Among the 1371 participants were 754 women and 617 men; 459 Hispanics, 383 African Americans, and 529 non-Hispanic whites; 437 with type 2 diabetes, 301 with impaired glucose tolerance, and 633 with normal glucose tolerance. The mean (SD) age was 55.5 (8.5) years, body mass index was 29.3 (5.8) kg/m(2), and S-1 was 1.6 (1.8) units. Adjusted for age, sex, and ethnicity, S, was not associated with LDL-C (r = 0.01); however, S, was associated with LDL size (r = 0.34, P < .001), LDL particle concentration (r = -0.28, P < .001), small LDL (r = -0.3, P < .001), intermediate LDL (r = -0.37, P < .001), and large LDL (r = 0.21, P < .001). In addition, S, was associated with TG (r = -0.36, P < .001), VLDL particles (r = -0.08, P < .01), large VLDL (r = -0.32, P < .001), VLDL size (r = -0.38, P < .001), HDL-C (r = 0.37, P < .001), HDL particles (r = 0.09, P < .001), large HDL (r = 0.31, P < .001), and HDL size (r = 0.33, P < .001). A factor analysis revealed a factor that accounted for 41.4% of the variance across the lipoprotein measures and that was correlated with S, (r = -0.33, P < .001). Similar results of opposing direction were observed for analyses of lipoprotein measures with fasting insulin and adiposity.Conclusions: The dyslipidemia associated with insulin resistance and obesity includes effects on lipoprotein metabolism that are missed when traditional lipoprotein cholesterol and total TG are examined. Lipoprotein size and subclasses should be examined in studies investigating the roles of insulin resistance and obesity in the pathogenesis and prevention of atherosclerosis. (C) 2005 Elsevier Inc. All rights reserved.