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脂肪酸去饱和酶(FADS)基因的遗传变异:对脂肪酸摄入饮食建议的影响

Genetic Variants in the FADS Gene: Implications for Dietary Recommendations for Fatty Acid Intake.

作者信息

Mathias Rasika A, Pani Vrindarani, Chilton Floyd H

机构信息

Division of Allergy and Clinical Immunology, Department of Medicine, The Johns Hopkins University, Baltimore, MD 21224, USA.

The Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest School of Medicine, Winston-Salem NC, 27157, USA ; Department of Physiology/Pharmacology, Wake Forest School of Medicine, Winston-Salem NC 27157, USA ; Molecular Medicine and Translational Sciences, Wake Forest School of Medicine, Winston-Salem NC 27157, USA.

出版信息

Curr Nutr Rep. 2014 Jun;3(2):139-148. doi: 10.1007/s13668-014-0079-1.

DOI:10.1007/s13668-014-0079-1
PMID:24977108
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4070521/
Abstract

Unequivocally, genetic variants within the fatty acid desaturase () cluster are determinants of long chain polyunsaturated fatty acid (LC-PUFA) levels in circulation, cells and tissues. A recent series of papers have addressed these associations in the context of ancestry; evidence clearly supports that the associations are robust to ethnicity. However ∼80% of African Americans carry two copies of the alleles associated with increased levels of arachidonic acid, compared to only ∼45% of European Americans raising important questions of whether gene-PUFA interactions induced by a modern western diet are differentially driving the risk of diseases of inflammation in diverse populations, and are these interactions leading to health disparities. We highlight an important aspect thus far missing in the debate regarding dietary recommendations; we content that current evidence from genetics strongly suggest that an individual's, or at the very least the population from which an individual is sampled, genetic architecture must be factored into dietary recommendations currently in place.

摘要

脂肪酸去饱和酶()基因簇内的遗传变异无疑是循环系统、细胞和组织中长链多不饱和脂肪酸(LC-PUFA)水平的决定因素。最近一系列论文在祖先背景下探讨了这些关联;证据明确支持这些关联不受种族影响。然而,约80%的非裔美国人携带与花生四烯酸水平升高相关的两个等位基因拷贝,相比之下,只有约45%的欧裔美国人携带,这就引发了重要问题:现代西方饮食诱导的基因与PUFA相互作用是否在不同人群中以不同方式驱动炎症性疾病风险,以及这些相互作用是否导致健康差异。我们强调了在关于饮食建议的辩论中迄今缺失的一个重要方面;我们认为,目前来自遗传学的证据有力地表明,在制定现行饮食建议时,必须考虑个体或至少是个体所来自人群的遗传结构。

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本文引用的文献

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Fatty acids and epigenetics.脂肪酸与表观遗传学。
Curr Opin Clin Nutr Metab Care. 2014 Mar;17(2):156-61. doi: 10.1097/MCO.0000000000000023.
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Dietary arachidonic acid and docosahexaenoic acid regulate liver fatty acid desaturase (FADS) alternative transcript expression in suckling piglets.膳食花生四烯酸和二十二碳六烯酸调节乳猪肝脏脂肪酸去饱和酶(FADS)替代转录物的表达。
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FADS2 Genetic Variance in Combination with Fatty Acid Intake Might Alter Composition of the Fatty Acids in Brain.FADS2基因变异与脂肪酸摄入相结合可能会改变大脑中脂肪酸的组成。
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Association of polymorphisms in FADS gene with age-related changes in serum phospholipid polyunsaturated fatty acids and oxidative stress markers in middle-aged nonobese men.FADS 基因多态性与中年非肥胖男性血清磷脂多不饱和脂肪酸与氧化应激标志物随年龄变化的相关性。
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