UMR 1280 Physiologie des Adaptations Nutritionnelles, INRA, Université de Nantes, CHU Nantes, Nantes, France.
Inflamm Bowel Dis. 2010 Apr;16(4):684-95. doi: 10.1002/ibd.21108.
The short-chain fatty acid butyrate, which is mainly produced in the lumen of the large intestine by the fermentation of dietary fibers, plays a major role in the physiology of the colonic mucosa. It is also the major energy source for the colonocyte. Numerous studies have reported that butyrate metabolism is impaired in intestinal inflamed mucosa of patients with inflammatory bowel disease (IBD). The data of butyrate oxidation in normal and inflamed colonic tissues depend on several factors, such as the methodology or the models used or the intensity of inflammation. The putative mechanisms involved in butyrate oxidation impairment may include a defect in beta oxidation, luminal compounds interfering with butyrate metabolism, changes in luminal butyrate concentrations or pH, and a defect in butyrate transport. Recent data show that butyrate deficiency results from the reduction of butyrate uptake by the inflamed mucosa through downregulation of the monocarboxylate transporter MCT1. The concomitant induction of the glucose transporter GLUT1 suggests that inflammation could induce a metabolic switch from butyrate to glucose oxidation. Butyrate transport deficiency is expected to have clinical consequences. Particularly, the reduction of the intracellular availability of butyrate in colonocytes may decrease its protective effects toward cancer in IBD patients.
短链脂肪酸丁酸盐主要由膳食纤维在大肠腔中发酵产生，在结肠黏膜生理学中起主要作用。它也是结肠细胞的主要能量来源。大量研究表明，炎症性肠病（IBD）患者的肠道炎症黏膜中丁酸盐代谢受损。正常和炎症结肠组织中丁酸盐氧化的数据取决于几个因素，例如所使用的方法学或模型或炎症的强度。丁酸盐氧化受损涉及的潜在机制可能包括β氧化缺陷、干扰丁酸盐代谢的腔化合物、腔内丁酸盐浓度或 pH 值变化以及丁酸盐转运缺陷。最近的数据表明，丁酸盐缺乏是由于炎症黏膜中通过下调单羧酸转运蛋白 MCT1 减少丁酸盐摄取所致。葡萄糖转运蛋白 GLUT1 的同时诱导表明炎症可能诱导从丁酸盐到葡萄糖氧化的代谢转换。预计丁酸盐转运缺陷会产生临床后果。特别是，结肠细胞内丁酸盐的可用性减少可能会降低其对 IBD 患者癌症的保护作用。
