Department of Gastroenterology, Portsmouth Hospitals NHS Trust, Portsmouth, United Kingdom.
Elsie Widdowson Laboratory, MRC Human Nutrition Research, Cambridge, United Kingdom; Nestle Institute of Health Sciences, 1015 Lausanne, Switzerland.
J Crohns Colitis. 2014 Jan;8(1):70-9. doi: 10.1016/j.crohns.2013.03.013. Epub 2013 Apr 23.
The polyunsaturated fatty acids (PUFA) arachidonic acid (AA, n-6) and eicosapentaenoic acid (EPA, n-3) are precursors of eicosanoids and other lipid mediators which have critical roles in inflammation. The mediators formed from the different PUFA have different potencies. We hypothesised that metabolic changes associated with colonic mucosal inflammation would modify the bioavailability of the eicosanoid precursors AA and EPA.
Colonic mucosa biopsies were obtained from patients with ulcerative colitis and from matched controls. Inflammation was graded endoscopically and histologically. Esterified and non-esterified fatty acids were determined within the biopsies using gas chromatography-mass spectrometry and liquid chromatography-mass spectrometry, respectively.
Biopsy samples were collected from 69 UC patients (54 providing both inflamed and non-inflamed mucosa) and 69 controls. Inflamed mucosa had higher AA (p<0.001) and lower EPA (p<0.010) contents and a higher AA:EPA ratio (p<0.001). Inflamed mucosa also had higher docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA) and lower linoleic acid (LA) and α-linolenic acid (α-LNA) contents (all p<0.001), compared to non-inflamed and controls. There were significant correlations between severity of inflammation and contents of AA, DPA and DHA (positive correlations) and of LA, α-LNA and EPA (negative correlations).
Higher AA, AA:EPA ratio, DPA and DHA and lower LA, α-LNA and EPA are seen in inflamed mucosa in UC and correlate with severity of inflammation. This suggests an alteration in fatty acid metabolism in the inflamed gut mucosa, which may offer novel targets for intervention and should be considered if nutritional strategies are used.
多不饱和脂肪酸（PUFA）花生四烯酸（AA，n-6）和二十碳五烯酸（EPA，n-3）是类二十烷酸和其他脂质介质的前体，这些介质在炎症中起着关键作用。不同 PUFA 形成的介质具有不同的效力。我们假设与结肠黏膜炎症相关的代谢变化会改变类二十烷酸前体 AA 和 EPA 的生物利用度。
从溃疡性结肠炎患者和匹配的对照中获取结肠黏膜活检。内镜和组织学分级炎症。使用气相色谱-质谱法和液相色谱-质谱法分别在活检中确定酯化和非酯化脂肪酸。
共采集了 69 例 UC 患者（54 例同时提供炎症和非炎症黏膜）和 69 例对照的活检样本。炎症黏膜 AA 含量较高（p<0.001），EPA 含量较低（p<0.010），AA:EPA 比值较高（p<0.001）。与非炎症和对照相比，炎症黏膜的二十二碳五烯酸（DPA）和二十二碳六烯酸（DHA）含量较高，亚油酸（LA）和α-亚麻酸（α-LNA）含量较低（均 p<0.001）。炎症严重程度与 AA、DPA 和 DHA 含量呈正相关（正相关），与 LA、α-LNA 和 EPA 含量呈负相关（负相关）。
在 UC 中，炎症黏膜中观察到 AA、AA:EPA 比值、DPA 和 DHA 升高，LA、α-LNA 和 EPA 降低，且与炎症严重程度相关。这表明炎症肠黏膜中脂肪酸代谢发生改变，可能为干预提供新的靶点，如果使用营养策略，应予以考虑。
