利用临床前模型深入了解炎症性肠病和膳食脂肪酸摄入量的影响,重点关注多不饱和脂肪酸。

Journal of the Canadian Association of Gastroenterology Pub Date : 2023-12-20 eCollection Date: 2024-02-01 DOI:10.1093/jcag/gwad058
Matthew Smyth, Genelle Lunken, Kevan Jacobson
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引用次数: 0

摘要

虽然炎症性肠病(IBD)的病因与遗传易感性和环境因素有关,但其潜在的分子机制仍不清楚。在环境因素中,饮食和肠道微生物群被认为是 IBD 免疫失调的驱动因素。事实上,流行病学研究强调,IBD 发病率的增加与膳食中欧米茄-6(n-6)多不饱和脂肪酸(PUFAs)摄入量的增加以及 n-6 脂肪酸与 n-3 脂肪酸摄入量平衡的变化相平行。实验证据表明,n-6 多不饱和脂肪酸摄入量的增加会增加细胞膜花生四烯酸,同时产生促炎症介质并增加氧化应激;这些因素共同导致了慢性炎症的发展。不过,越来越清楚的是,一些 n-6 PUFA 衍生介质会根据摄入的环境和时间产生有益的影响。与 n-6 相反,当 n-3 PUFA 二十碳五烯酸和二十二碳六烯酸被纳入细胞膜并代谢成较少的促炎症类二十烷酸,以及强效的专业促溶解介质时,它们在炎症停止中发挥作用。我们以临床前模型为重点,探索膳食脂质、肠道微生物组和肠道炎症之间的关系。
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Insights Into Inflammatory Bowel Disease and Effects of Dietary Fatty Acid Intake With a Focus on Polyunsaturated Fatty Acids Using Preclinical Models.

While the aetiology of inflammatory bowel disease (IBD) has been linked to genetic susceptibility coupled with environmental factors, the underlying molecular mechanisms remain unclear. Among the environmental factors, diet and the gut microbiota have been implicated as drivers of immune dysregulation in IBD. Indeed, epidemiologic studies have highlighted that the increase in incidence of IBD parallels the increase in dietary intake of omega-6 (n-6) polyunsaturated fatty acids (PUFAs) and the change in balance of intake of n-6 to n-3 fatty acids. Experimental evidence suggests that the increase in n-6 PUFA intake increases cell membrane arachidonic acid, which is accompanied by the production of pro-inflammatory mediators as well as increased oxidative stress; together, this contributes to the development of chronic inflammation. However, it is also increasingly clear that some of the n-6 PUFA-derived mediators exert beneficial effects depending on the settings and timing of ingestion. In contrast to n-6, when n-3 PUFA eicosapentaenoic acid and docosahexaenoic acid are incorporated into the cell membrane and are metabolized into less pro-inflammatory eicosanoids, as well as strong specialized pro-resolving mediators, which play a role in inflammation cessation. With a focus on preclinical models, we explore the relationship between dietary lipid, the gut microbiome, and intestinal inflammation.

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