高血脂以及由此引發(fā)的心臟病已成為現(xiàn)代人的一大困擾,，除生活習(xí)慣外,，高血脂與遺傳也有關(guān)系。一項最新研究剛剛確認(rèn)了近百個會增加高血脂風(fēng)險的基因,，這將有助于從小通過基因檢測來預(yù)測高血脂并提前采取防治措施,。
新一期英國《自然》(Nature )雜志刊登報告說，美英德等多國研究人員聯(lián)手進(jìn)行了迄今最大規(guī)模的高血脂基因研究,，通過分析約10萬名志愿者的基因,，確定了95個與高血脂風(fēng)險有關(guān)的基因，其中59個是第一次發(fā)現(xiàn),。研究顯示,，攜帶這些基因的人出現(xiàn)高血脂的風(fēng)險是其他人的14倍,。
英國愛丁堡大學(xué)的研究人員詹姆斯·威爾遜說，在確認(rèn)這么多與高血脂風(fēng)險有關(guān)的基因后,，人們首次可以通過基因分析來預(yù)測誰更可能出現(xiàn)高血脂,，由于基因分析在小時候就可以進(jìn)行,，這將有助于那些高風(fēng)險者提前采取措施控制血脂,，盡量避免由此引起心臟病。
血脂是血液中膽固醇和甘油三酯等物質(zhì)的總稱,，如果血脂含量過高,，脂肪可能會在血管內(nèi)沉積，引起動脈粥樣硬化,，并最終導(dǎo)致心臟病,。（生物谷Bioon.com）
生物谷推薦原文出處：
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.
