JAHA：高密度脂蛋白可能并不防止心脏疾病

一项由哈佛大学公共卫生学院（HSPH）研究人员完成的研究证实：所谓的“好”胆固醇--高密度脂蛋白（HDL）胆固醇可能无法防止冠状动脉心脏疾病（CHD ）的发生，实际上可能是有害的。

这是首次有研究表明一个小蛋白，载脂蛋白C-III（载脂蛋白C-III），有时存在于高密度脂蛋白胆固醇表面上，可能会增加心脏疾病的风险，没有高密度脂蛋白胆固醇可能对心脏有保护作用。

这项研究结果发表在Journal of the American Heart Association杂志上。

哈佛大学公共卫生Frank Sacks教授说，如果在正在进行的研究得到证实，这一发现可能会导致更好的评估个人心脏疾病的风险和更精确的靶向治疗，以提高保护HDL或降低不利的高密度脂蛋白胆固醇与载脂蛋白C-III预防心血管疾病。

高密度脂蛋白胆固醇水平是冠状动脉心脏疾病（CHD）发病率较低的预测指标。但是增加高密度脂蛋白胆固醇的药物试验并没有始终显示能降低高密度脂蛋白胆固醇，导致高密度脂蛋白胆固醇可能含有保护和非保护元件假设的产生。

载脂蛋白C-III是一种炎症蛋白，驻留在一些脂蛋白高密度脂蛋白胆固醇和低密度脂蛋白、低密度脂蛋白（“坏”胆固醇）的表面。哈佛大学公共卫生营养系Sacks和Majken Jensen研究人员研究载脂蛋白C- III是否存在的情况下对有心脏保护特质的高密度脂蛋白胆固醇的影响，以及是否它的存在可以区分高密度脂蛋白胆固醇为两个子类，哪些能抵御未来心脏疾病的风险，哪些不能。

研究人员对1989年和1990年参与布里格姆妇女医院的护士健康研究的参试者进行了审查，连同从1993年至1995年收集的18,225男子血液样本，收集32826妇女的血液样本。

研究人员比较了无载脂蛋白C-III总高密度脂蛋白（HDL）、高密度脂蛋白胆固醇、载脂蛋白C-III、高密度脂蛋白的血浆浓度作为预测冠心病的危险。

结果表明相比于测量的高密度脂蛋白胆固醇载脂蛋白C-III和无载脂蛋白C-III高密度脂蛋白，总HDL可能更好的预测心脏疾病的风险。高密度脂蛋白、载脂蛋白C-III有可能成为治疗疗效的指标。（生物谷：Bioon.com）

doi:10.1161/​JAHA.111.000232
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Apolipoprotein C-III as a Potential Modulator of the Association Between HDL-Cholesterol and Incident Coronary Heart Disease

Majken K. Jensen, PhD; Eric B. Rimm, ScD; Jeremy D. Furtado, ScD; Frank M. Sacks, ScD

Background High-density lipoproteins (HDL) are structurally and metabolically heterogeneous and subclasses with differential effects on coronary heart disease (CHD) might exist. Apolipoprotein (apo) C-III, a small proinflammatory protein that resides on the surface of lipoproteins, enhances the atherogenicity of VLDL and LDL particles, but little is known about the role apoC-III on HDL. We investigated whether the presence or absence of apoC-III differentiates HDL into subtypes with nonprotective or protective associations with risk of future CHD.

Methods and Results High-density lipoprotein cholesterol (HDL-C) levels were measured in plasma separated according to apoC-III (by immunoaffinity chromatography) in two prospective case-control studies nested within the Nurses’ Health and the Health Professionals Follow-Up Studies. Baseline was in 1990 and 1994, and 634 incident CHD cases were documented through 10 to 14 years of follow-up. The relative risk of CHD per each standard deviation of total HDL-C was 0.78 (95% confidence intervals, 0.63–0.96). The HDL-C subtypes were differentially associated with risk of CHD, HDL-C without apoC-III inversely and HDL-C with apoC-III directly (P=0.02 for a difference between the HDL types). The relative risk per standard deviation of HDL-C without apoC-III was 0.66 (0.53 to 0.93) and 1.18 (1.03 to 1.34) for HDL-C with apoC-III. HDL-C with apoC-III comprised ∼13% of the total HDL-C. Adjustment for triglycerides and apoB attenuated the risks; however, the two HDL-C subgroups remained differentially associated with risk of CHD (P=0.05).

Conclusion Separating HDL-C according to apoC-III identified two types of HDL with opposing associations with risk of CHD. The proatherogenic effects of apoC-III, as a component of VLDL and LDL, may extend to HDL.