从头合成途径中的脂肪酸与冠心病风险：心血管健康研究。
Fatty acids in the de novo lipogenesis pathway and risk of coronary heart disease: the Cardiovascular Health Study.
机构信息
Division of Cardiovascular Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
出版信息
Am J Clin Nutr. 2011 Aug;94(2):431-8. doi: 10.3945/ajcn.111.012054. Epub 2011 Jun 22.
BACKGROUND
De novo lipogenesis (DNL) is an endogenous pathway whereby carbohydrates and proteins are converted to fatty acids. DNL could affect coronary heart disease (CHD) or sudden cardiac arrest (SCA) via generation of specific fatty acids. Whether these fatty acids are prospectively associated with SCA or other CHD events is unknown.
OBJECTIVE
The objective was to investigate the relations of 4 fatty acids in the DNL pathway-palmitic acid (16:0), palmitoleic acid (16:1n-7), 7-hexadecenoic acid (16:1n-9), and cis-vaccenic acid (18:1n-7)-with incident CHD, including fatal CHD, nonfatal myocardial infarction (NFMI), and SCA.
DESIGN
A community-based prospective study was conducted in 2890 men and women aged ≥65 y, who were free of known CHD at baseline and who were followed from 1992 to 2006. Cardiovascular disease risk factors and plasma phospholipid fatty acids were measured at baseline by using standardized methods. Incident CHD was ascertained prospectively and was centrally adjudicated by using medical records. Risk was assessed by using multivariable-adjusted Cox proportional hazards.
RESULTS
During 29,835 person-years of follow-up, 631 CHD and 71 SCA events occurred. Both 18:1n-7 and 16:1n-9 were associated with a higher risk of SCA [multivariable-adjusted hazard ratio (95% CI) for the interquintile range: 7.63 (2.58, 22.6) for 18:1n-7 and 2.30 (1.16, 4.55) for 16:1n-9] but not of total CHD, fatal CHD, or NFMI. In secondary analyses censored to mid-follow-up (7 y) to minimize the effects of changes in concentrations over time, 16:1n-9 was also associated with a significantly higher risk of total CHD (2.11; 1.76, 2.54), including a higher risk of CHD death, NFMI, and SCA; 16:0 and 16:1n-7 were not associated with clinical CHD outcomes.
CONCLUSION
Higher plasma phospholipid 18:1n-7 and 16:1n-9 concentrations were prospectively associated with an elevated risk of SCA but not of other CHD events, except in secondary analyses.
背景
从头合成脂肪生成（DNL）是一种内源性途径，通过该途径，碳水化合物和蛋白质可转化为脂肪酸。DNL 可能会通过产生特定的脂肪酸来影响冠心病（CHD）或心源性猝死（SCA）。这些脂肪酸是否与 SCA 或其他 CHD 事件有前瞻性关联尚不清楚。
目的
本研究旨在调查从头合成脂肪生成途径中的 4 种脂肪酸——棕榈酸（16:0）、棕榈油酸（16:1n-7）、7-十六碳烯酸（16:1n-9）和顺式-十八碳烯酸（18:1n-7）——与冠心病事件（包括致命性冠心病、非致死性心肌梗死和 SCA）的关系。
设计
这是一项基于社区的前瞻性研究，研究对象为 2890 名年龄≥65 岁的男性和女性，他们在基线时无已知冠心病，随访时间从 1992 年持续到 2006 年。采用标准化方法在基线时测量心血管疾病风险因素和血浆磷脂脂肪酸。前瞻性确定冠心病事件，并通过医疗记录进行中心裁决。采用多变量调整的 Cox 比例风险评估风险。
结果
在 29835 人年的随访期间，发生了 631 例冠心病和 71 例 SCA 事件。18:1n-7 和 16:1n-9 与 SCA 风险升高相关（五分位间距内的多变量调整后的危险比（95%CI）：18:1n-7 为 7.63（2.58，22.6），16:1n-9 为 2.30（1.16，4.55）），但与总冠心病、致命性冠心病或非致死性心肌梗死无关。在次要分析中，为了尽量减少时间变化对浓度的影响，将随访时间（7 年）中值截断，结果显示，16:1n-9 与总冠心病（2.11；1.76，2.54）风险显著升高相关，包括冠心病死亡、非致死性心肌梗死和 SCA 的风险升高；16:0 和 16:1n-7 与临床冠心病结局无关。
结论
较高的血浆磷脂 18:1n-7 和 16:1n-9 浓度与 SCA 风险升高相关，但与其他冠心病事件无关，除了在次要分析中。
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