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本文引用的文献

1
The role of adipose tissue immune cells in obesity and low-grade inflammation.脂肪组织免疫细胞在肥胖和低度炎症中的作用。
J Endocrinol. 2014 Sep;222(3):R113-27. doi: 10.1530/JOE-14-0283. Epub 2014 Jul 8.
2
Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis.膳食、循环和补充脂肪酸与冠心病风险的关联:系统评价和荟萃分析。
Ann Intern Med. 2014 Mar 18;160(6):398-406. doi: 10.7326/M13-1788.
3
Redox-dependent anti-inflammatory signaling actions of unsaturated fatty acids.不饱和脂肪酸的氧化还原依赖的抗炎信号作用。
Annu Rev Physiol. 2014;76:79-105. doi: 10.1146/annurev-physiol-021113-170341. Epub 2013 Oct 16.
4
Genomic responses in mouse models poorly mimic human inflammatory diseases.小鼠模型中的基因组反应与人类炎症性疾病的反应相差很大。
Proc Natl Acad Sci U S A. 2013 Feb 26;110(9):3507-12. doi: 10.1073/pnas.1222878110. Epub 2013 Feb 11.
5
Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis.利用膳食亚油酸进行冠心病二级预防和死亡的评估:对悉尼饮食心脏研究中恢复数据的评估和更新的荟萃分析。
BMJ. 2013 Feb 4;346:e8707. doi: 10.1136/bmj.e8707.
6
A consideration of biomarkers to be used for evaluation of inflammation in human nutritional studies.考虑用于评估人类营养研究中炎症的生物标志物。
Br J Nutr. 2013 Jan;109 Suppl 1:S1-34. doi: 10.1017/S0007114512005119.
7
Dietary oil composition differentially modulates intestinal endotoxin transport and postprandial endotoxemia.饮食中的油脂成分可改变肠道内毒素的转运并影响餐后内毒素血症。
Nutr Metab (Lond). 2013 Jan 10;10(1):6. doi: 10.1186/1743-7075-10-6.
8
Impact of soluble epoxide hydrolase and epoxyeicosanoids on human health.可溶性环氧化物水解酶和环氧二十碳三烯酸对人类健康的影响。
Annu Rev Pharmacol Toxicol. 2013;53:37-58. doi: 10.1146/annurev-pharmtox-011112-140244. Epub 2012 Sep 27.
9
Effect of dietary linoleic acid on markers of inflammation in healthy persons: a systematic review of randomized controlled trials.膳食亚油酸对健康人群炎症标志物的影响:系统评价随机对照试验。
J Acad Nutr Diet. 2012 Jul;112(7):1029-41, 1041.e1-15. doi: 10.1016/j.jand.2012.03.029.
10
The outliers become a stampede as immunometabolism reaches a tipping point.免疫代谢达到临界点时,离群值就会成为蜂拥而至的趋势。
Immunol Rev. 2012 Sep;249(1):253-75. doi: 10.1111/j.1600-065X.2012.01142.x.

脂肪酸与炎症的科学。

The science of fatty acids and inflammation.

作者信息

Fritsche Kevin L

机构信息

Animal Sciences Division, Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO

出版信息

Adv Nutr. 2015 May 15;6(3):293S-301S. doi: 10.3945/an.114.006940. Print 2015 May.

DOI:10.3945/an.114.006940
PMID:25979502
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4424767/
Abstract

Inflammation is believed to play a central role in many of the chronic diseases that characterize modern society. In the past decade, our understanding of how dietary fats affect our immune system and subsequently our inflammatory status has grown considerably. There are compelling data showing that high-fat meals promote endotoxin [e.g., lipopolysaccharide (LPS)] translocation into the bloodstream, stimulating innate immune cells and leading to a transient postprandial inflammatory response. The nature of this effect is influenced by the amount and type of fat consumed. The role of various dietary constituents, including fats, on gut microflora and subsequent health outcomes in the host is another exciting and novel area of inquiry. The impact of specific fatty acids on inflammation may be central to how dietary fats affect health. Three key fatty acid-inflammation interactions are briefly described. First, the evidence suggests that saturated fatty acids induce inflammation in part by mimicking the actions of LPS. Second, the often-repeated claim that dietary linoleic acid promotes inflammation was not supported in a recent systematic review of the evidence. Third, an explanation is offered for why omega-3 (n-3) polyunsaturated fatty acids are so much less anti-inflammatory in humans than in mice. The article closes with a cautionary tale from the genomic literature that illustrates why extrapolating the results from inflammation studies in mice to humans is problematic.

摘要

炎症被认为在现代社会诸多慢性疾病中起着核心作用。在过去十年里,我们对膳食脂肪如何影响免疫系统以及随后的炎症状态的理解有了显著进展。有令人信服的数据表明,高脂肪餐会促使内毒素(如脂多糖,LPS)转移到血液中,刺激先天免疫细胞并引发短暂的餐后炎症反应。这种效应的性质受所摄入脂肪的量和类型影响。包括脂肪在内的各种膳食成分对肠道微生物群以及宿主随后健康状况的作用是另一个令人兴奋的新研究领域。特定脂肪酸对炎症的影响可能是膳食脂肪影响健康的核心所在。本文简要描述了三种关键的脂肪酸与炎症的相互作用。首先,有证据表明饱和脂肪酸部分通过模拟LPS的作用来诱发炎症。其次,最近对证据的系统评价并不支持膳食亚油酸会促进炎症这一常被提及的说法。第三,文中解释了为什么ω-3(n-3)多不饱和脂肪酸在人类中的抗炎作用远不如在小鼠中明显。文章最后讲述了一个来自基因组学文献的警示故事,说明了为何将小鼠炎症研究结果外推至人类存在问题。