Lamarche B, Lemieux I, Després J P
Department of Food Sciences and Nutrition, Laval University, Ste-Foy, Québec, Canada.
Diabetes Metab. 1999 Sep;25(3):199-211.
More than decade ago, several cross-sectional studies have reported differences in LDL particle size, density and composition between coronary heart disease (CHD) patients and healthy controls. Three recent prospective, nested case-control studies have since confirmed that the presence of small, dense LDL particles was associated with more than a three-fold increase in the risk of CHD. The small, dense LDL phenotype rarely occurs as an isolated disorder. It is most frequently accompanied by hypertriglyceridemia, reduced HDL cholesterol levels, abdominal obesity, insulin resistance and by a series of other metabolic alterations predictive of an impaired endothelial function and increased susceptibility to thrombosis. Whether or not the small, dense LDL phenotype should be considered an independent CHD risk factor remains to be clearly established. The cluster of metabolic abnormalities associated with small, dense LDL particles has been referred to as the insulin resistance-dyslipidemic phenotype of abdominal obesity. Results from the Québec Cardiovascular Study have indicated that individuals displaying three of the numerous features of insulin resistance (elevated plasma insulin and apolipoprotein B concentrations and small, dense LDL particles) showed a remarkable increase in CHD risk. Our data suggest that the increased risk of CHD associated with having small, dense LDL particles may be modulated to a significant extent by the presence/absence of insulin resistance, abdominal obesity and increased LDL particle concentration. We suggest that the complex interactions among the metabolic alterations of the insulin resistance syndrome should be considered when evaluating the risk of CHD associated with the small, dense LDL phenotype. From a therapeutic standpoint, the treatment of this condition should not only aim at reducing plasma triglyceride levels, but also at improving all features of the insulin resistance syndrome, for which body weight loss and mobilization of abdominal fat appear as key elements. Finally, interventions leading to reduction in fasting triglyceride levels will increase LDL particle size and contribute to reduce CHD risk, particularly if plasma apolipoprotein B concentration (as a surrogate of the number of atherogenic particles) is also reduced.
十多年前，几项横断面研究报告了冠心病（CHD）患者与健康对照者之间低密度脂蛋白（LDL）颗粒大小、密度和组成的差异。此后，最近的三项前瞻性巢式病例对照研究证实，小而密的LDL颗粒的存在与冠心病风险增加三倍以上相关。小而密的LDL表型很少作为一种孤立的病症出现。它最常伴有高甘油三酯血症、高密度脂蛋白胆固醇水平降低、腹部肥胖、胰岛素抵抗以及一系列其他代谢改变，这些改变预示着内皮功能受损和血栓形成易感性增加。小而密的LDL表型是否应被视为独立的冠心病危险因素仍有待明确确定。与小而密的LDL颗粒相关的代谢异常集群被称为腹部肥胖的胰岛素抵抗 - 血脂异常表型。魁北克心血管研究的结果表明，表现出胰岛素抵抗众多特征中的三项（血浆胰岛素和载脂蛋白B浓度升高以及小而密的LDL颗粒）的个体冠心病风险显著增加。我们的数据表明，与小而密的LDL颗粒相关的冠心病风险增加在很大程度上可能会受到胰岛素抵抗、腹部肥胖和LDL颗粒浓度增加与否的调节。我们建议，在评估与小而密的LDL表型相关的冠心病风险时，应考虑胰岛素抵抗综合征代谢改变之间的复杂相互作用。从治疗角度来看，这种病症的治疗不仅应旨在降低血浆甘油三酯水平，还应旨在改善胰岛素抵抗综合征的所有特征，其中体重减轻和腹部脂肪动员似乎是关键因素。最后，导致空腹甘油三酯水平降低的干预措施将增加LDL颗粒大小并有助于降低冠心病风险，特别是如果血浆载脂蛋白B浓度（作为致动脉粥样硬化颗粒数量的替代指标）也降低的话。
