LDL SUBCLASS PHENOTYPES AND TRIGLYCERIDE-METABOLISM IN NON-INSULIN-DEPENDENT DIABETES
LDL SUBCLASS PHENOTYPES AND TRIGLYCERIDE-METABOLISM IN NON-INSULIN-DEPENDENT DIABETES
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DOI：
10.1161/01.atv.12.12.1496
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发表时间：
1992-12-01
期刊：
影响因子：
--
通讯作者：
KRAUSS, RM
中科院分区：
文献类型：
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作者：
FEINGOLD, KR;GRUNFELD, C;KRAUSS, RM
血浆低密度脂蛋白（LDL）包括大小、密度和化学组成不同的多个离散亚类。一种常见的可遗传表型，其特征是小而致密的LDL颗粒占优势（LDL亚类表型B），与具有较大LDL（LDL亚类表型A）的受试者相比，与血浆甘油三酯浓度相对升高、高密度脂蛋白水平降低和冠状动脉疾病风险增加相关。群体研究表明，大约20-30%的成年男性具有表型B，另外15-20%具有中等大小的LDL。表型B中的脂质变化与非胰岛素依赖型糖尿病（NIDDM）患者中观察到的脂质变化相似。在本研究中，我们评估了血脂正常的NIDDM男性和年龄匹配的血脂水平相似的对照组的LDL亚类表型。在NIDDM受试者中，LDL B表型个体的百分比增加了两倍以上。在NIDDM受试者中，与LDL A表型相比，LDL B表型与更高的血浆甘油三酯水平和更低的高密度脂蛋白胆固醇水平的趋势相关，正如先前在对照组中观察到的那样。糖尿病控制指标，如空腹和血红蛋白A1水平，无论LDL表型模式如何，都是相似的，这表明血糖控制不太可能解释LDL B表型的增加。在对照组和NIDDM受试者中，LDL表型B的受试者中富含甘油三酯的脂蛋白的清除比表型A的受试者慢。多元回归分析表明NIDDM的诊断是LDL B表型的独立预测因子。总之，本研究表明，NIDDM与LDL亚类表型B的患病率增加有关，即使没有明显的高脂血症。因此，遗传和代谢因素导致的优势小，密度低密度脂蛋白可能有助于增加血管疾病的风险与NIDDM患者。
Plasma low density lipoprotein (LDL) comprises multiple discrete subclasses differing in size, density, and chemical composition. A common, heritable phenotype characterized by the predominance of small, dense LDL particles (LDL subclass phenotype B) is associated with relatively increased concentrations of plasma triglycerides, reduced levels of high density lipoprotein, and increased risk of coronary artery disease in comparison with subjects with larger LDL (LDL subclass phenotype A). Population studies have indicated that approximately 20-30% of adult men have phenotype B, and another 15-20% have LDL of intermediate size. The lipid changes in phenotype B are similar to those that have been observed in patients with non-insulin-dependent diabetes mellitus (NIDDM). In the present study, we have assessed LDL subclass phenotypes in normolipidemic men with NIDDM and in age-matched control subjects who had similar lipid levels. There was a greater than twofold increase in the percentage of individuals with the LDL B phenotype in the NIDDM subjects. The LDL B phenotype was associated with higher plasma triglyceride levels and a trend toward lower high density lipoprotein cholesterol levels compared with the LDL A phenotype in the NIDDM subjects, as has been previously observed in control groups. Indices of diabetic control, such as fasting and hemoglobin A1 levels, were similar regardless of LDL phenotype pattern, suggesting that glycemic control was not likely to account for the increase in the LDL B phenotype. In both control and NIDDM subjects, the clearance of triglyceride-rich lipoproteins was slowed in the subjects with the LDL phenotype B compared with those with the A phenotype. Multiple regression analysis demonstrated that the diagnosis of NIDDM is an independent predictor of the LDL B phenotype. In summary, the present study demonstrates that NIDDM is associated with an increased prevalence of the LDL subclass phenotype B, even in the absence of frank hyperlipidemia. Thus, genetic and metabolic factors leading to the predominance of small, dense LDL may contribute to the increased risk of vascular disease in patients with NIDDM.