高血脂以及由此引发的心脏病已成为现代人的一大困扰，除生活习惯外，高血脂与遗传也有关系。一项最新研究刚刚确认了近百个会增加高血脂风险的基因，这将有助于从小通过基因检测来预测高血脂并提前采取防治措施。
新一期英国《自然》(Nature )杂志刊登报告说，美英德等多国研究人员联手进行了迄今最大规模的高血脂基因研究，通过分析约10万名志愿者的基因，确定了95个与高血脂风险有关的基因，其中59个是第一次发现。研究显示，携带这些基因的人出现高血脂的风险是其他人的14倍。
英国爱丁堡大学的研究人员詹姆斯·威尔逊说，在确认这么多与高血脂风险有关的基因后，人们首次可以通过基因分析来预测谁更可能出现高血脂，由于基因分析在小时候就可以进行，这将有助于那些高风险者提前采取措施控制血脂，尽量避免由此引起心脏病。
血脂是血液中胆固醇和甘油三酯等物质的总称，如果血脂含量过高，脂肪可能会在血管内沉积，引起动脉粥样硬化，并最终导致心脏病。（生物谷Bioon.com）
生物谷推荐原文出处：
Nature doi:10.1038/nature09270
Biological, clinical and population relevance of 95 loci for blood lipids
Tanya M. Teslovich,Kiran Musunuru,Albert V. Smith,Andrew C. Edmondson,Ioannis M. Stylianou,Masahiro Koseki,James P. Pirruccello,Samuli Ripatti,Daniel I. Chasman,Cristen J. Willer,Christopher T. Johansen,Sigrid W. Fouchier,Aaron Isaacs,Gina M. Peloso,Maja Barbalic,Sally L. Ricketts,Joshua C. Bis,Yurii S. Aulchenko,Gudmar Thorleifsson,Mary F. Feitosa,John Chambers,Marju Orho-Melander,Olle Melander,Toby Johnson,Xiaohui Li,et al
Plasma concentrations of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides are among the most important risk factors for coronary artery disease (CAD) and are targets for therapeutic intervention. We screened the genome for common variants associated with plasma lipids in >100,000 individuals of European ancestry. Here we report 95 significantly associated loci (P?<?5?×?10?8), with 59 showing genome-wide significant association with lipid traits for the first time. The newly reported associations include single nucleotide polymorphisms (SNPs) near known lipid regulators (for example, CYP7A1, NPC1L1 and SCARB1) as well as in scores of loci not previously implicated in lipoprotein metabolism. The 95 loci contribute not only to normal variation in lipid traits but also to extreme lipid phenotypes and have an impact on lipid traits in three non-European populations (East Asians, South Asians and African Americans). Our results identify several novel loci associated with plasma lipids that are also associated with CAD. Finally, we validated three of the novel genes—GALNT2, PPP1R3B and TTC39B—with experiments in mouse models. Taken together, our findings provide the foundation to develop a broader biological understanding of lipoprotein metabolism and to identify new therapeutic opportunities for the prevention of CAD.
