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饮食-基因相互作用与多不饱和脂肪酸代谢:导致健康差异和人类疾病的潜在因素。

Diet-gene interactions and PUFA metabolism: a potential contributor to health disparities and human diseases.

机构信息

The Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.

Department of Pharmacology, University of Colorado Denver, Aurora, CO 80045, USA.

出版信息

Nutrients. 2014 May 21;6(5):1993-2022. doi: 10.3390/nu6051993.

DOI:10.3390/nu6051993
PMID:24853887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4042578/
Abstract

The "modern western" diet (MWD) has increased the onset and progression of chronic human diseases as qualitatively and quantitatively maladaptive dietary components give rise to obesity and destructive gene-diet interactions. There has been a three-fold increase in dietary levels of the omega-6 (n-6) 18 carbon (C18), polyunsaturated fatty acid (PUFA) linoleic acid (LA; 18:2n-6), with the addition of cooking oils and processed foods to the MWD. Intense debate has emerged regarding the impact of this increase on human health. Recent studies have uncovered population-related genetic variation in the LCPUFA biosynthetic pathway (especially within the fatty acid desaturase gene (FADS) cluster) that is associated with levels of circulating and tissue PUFAs and several biomarkers and clinical endpoints of cardiovascular disease (CVD). Importantly, populations of African descent have higher frequencies of variants associated with elevated levels of arachidonic acid (ARA), CVD biomarkers and disease endpoints. Additionally, nutrigenomic interactions between dietary n-6 PUFAs and variants in genes that encode for enzymes that mobilize and metabolize ARA to eicosanoids have been identified. These observations raise important questions of whether gene-PUFA interactions are differentially driving the risk of cardiovascular and other diseases in diverse populations, and contributing to health disparities, especially in African American populations.

摘要

“现代西方”饮食(MWD)增加了慢性人类疾病的发病和进展,因为定性和定量不适宜的饮食成分导致肥胖和破坏性的基因-饮食相互作用。MWD 中ω-6(n-6)18 碳多不饱和脂肪酸(PUFA)亚油酸(LA;18:2n-6)的饮食水平增加了两倍,这是由于烹饪油和加工食品的加入。关于这种增加对人类健康的影响,出现了激烈的争论。最近的研究揭示了人群相关的 LCPUFA 生物合成途径中的遗传变异(特别是脂肪酸去饱和酶基因(FADS)簇内),与循环和组织 PUFA 以及几种心血管疾病(CVD)的生物标志物和临床终点相关。重要的是,非洲裔人群中与花生四烯酸(ARA)水平升高、CVD 生物标志物和疾病终点相关的变异的频率更高。此外,还确定了膳食 n-6 PUFA 与编码动员和代谢 ARA 为类二十烷酸的酶的基因之间的营养基因组相互作用。这些观察结果提出了一个重要的问题,即基因-PUFA 相互作用是否在不同人群中以不同的方式驱动心血管和其他疾病的风险,并导致健康差异,尤其是在非裔美国人中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1376/4042578/a72105d22b48/nutrients-06-01993-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1376/4042578/a01be40bc91d/nutrients-06-01993-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1376/4042578/1f1eab2403fa/nutrients-06-01993-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1376/4042578/93144dd4b3d3/nutrients-06-01993-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1376/4042578/a72105d22b48/nutrients-06-01993-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1376/4042578/a01be40bc91d/nutrients-06-01993-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1376/4042578/1f1eab2403fa/nutrients-06-01993-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1376/4042578/93144dd4b3d3/nutrients-06-01993-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1376/4042578/a72105d22b48/nutrients-06-01993-g004.jpg

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