Fritsche Kevin L
Animal Sciences Division, Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO
Adv Nutr. 2015 May 15;6(3):293S-301S. doi: 10.3945/an.114.006940. Print 2015 May.
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.
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。