Crohn’s disease and ulcerative colitis, phenotypically comprising a spectrum of inflammatory bowel diseases (IBDs), spread globally during the westernization of lifestyle and dietary habits over the past few decades. Here, we review experimental and clinical evidence for the metabolic nature of gut inflammation in IBD and delineate distinct parallels to the inflammatory state in metabolic diseases. Experimental evidence indicates that excessive intake of specific macronutrients in a Western diet fuels an inflammatory response in the gut by exploiting sensors of innate immunity and perturbation of gut microbial metabolism. Genetic IBD risk partly affects metabolism and stress signalling of innate immunity, and immunometabolism controls susceptibility to gut inflammation. Epidemiological and clinical studies indicate that specific nutrients in the Western diet pose a risk for the development of IBD and a poor disease course. Translational studies in IBD indicate perturbation of energy metabolism in immune cells and perturbation of gut microbial metabolism, which can be shaped by diet. In turn, dietary restriction by exclusive enteral nutrition induces remission in patients with IBD. Collectively, these studies support a metabolic underpinning of gut inflammation in IBD as described for metabolic inflammation in obesity and related disorders.

克罗恩病和溃疡性结肠炎，表型包括一系列炎症性肠病 (IBD)，在过去几十年的生活方式和饮食习惯西化过程中在全球范围内传播。在这里，我们回顾了 IBD 中肠道炎症代谢性质的实验和临床证据，并描述了与代谢疾病中炎症状态的明显相似之处。实验证据表明，在西方饮食中过量摄入特定常量营养素会利用先天免疫传感器和肠道微生物代谢紊乱，从而加剧肠道炎症反应。遗传性 IBD 风险部分影响先天免疫的代谢和应激信号，而免疫代谢控制对肠道炎症的易感性。流行病学和临床研究表明，西方饮食中的特定营养素对 IBD 的发展和较差的病程构成风险。IBD 的转化研究表明免疫细胞能量代谢的扰动和肠道微生物代谢的扰动，这可以通过饮食来塑造。反过来，完全肠内营养的饮食限制可诱导 IBD 患者的病情缓解。总的来说，这些研究支持 IBD 中肠道炎症的代谢基础，如肥胖和相关疾病中的代谢性炎症所述。完全肠内营养的饮食限制可诱导 IBD 患者的缓解。总的来说，这些研究支持 IBD 中肠道炎症的代谢基础，如肥胖和相关疾病中的代谢性炎症所述。完全肠内营养的饮食限制可诱导 IBD 患者的缓解。总的来说，这些研究支持 IBD 中肠道炎症的代谢基础，如肥胖和相关疾病中的代谢性炎症所述。