Colgan Sean P, Wang Ruth X, Hall Caroline H T, Bhagavatula Geetha, Lee J Scott
Department of Medicine and the Mucosal Inflammation Program, University of Colorado School of Medicine, Aurora, CO, USA.
Rocky Mountain Veterans Hospital, Aurora, CO, USA.
Immunometabolism (Cobham). 2023 Jan 10;5(1):e0016. doi: 10.1097/IN9.0000000000000016. eCollection 2023 Jan.
Active episodes of inflammatory bowel disease (IBD), which include ulcerative colitis and Crohn's disease, coincide with profound shifts in the composition of the microbiota and host metabolic energy demand. Intestinal epithelial cells (IEC) that line the small intestine and colon serve as an initial point for contact for the microbiota and play a central role in innate immunity. In the 1980s, Roediger et al proposed the hypothesis that IBD represented a disease of diminished mucosal nutrition and energy deficiency ("starved gut") that strongly coincided with the degree of inflammation. These studies informed the scientific community about the important contribution of microbial-derived metabolites, particularly short-chain fatty acids (SCFA) such as butyrate, to overall energy homeostasis. Decades later, it is appreciated that disease-associated shifts in the microbiota, termed dysbiosis, places inordinate demands on energy acquisition within the mucosa, particularly during active inflammation. Here, we review the topic of tissue energetics in mucosal health and disease from the original perspective of that proposed by the starved gut hypothesis.
炎症性肠病（IBD）的活动期，包括溃疡性结肠炎和克罗恩病，与微生物群组成的深刻变化以及宿主代谢能量需求相吻合。排列在小肠和结肠内的肠上皮细胞（IEC）是微生物群接触的起始点，在先天免疫中起核心作用。20世纪80年代，罗伊迪格等人提出了一个假说，即IBD代表一种黏膜营养减少和能量缺乏的疾病（“饥饿肠道”），这与炎症程度密切相关。这些研究让科学界了解到微生物衍生代谢产物，特别是短链脂肪酸（SCFA）如丁酸盐对整体能量稳态的重要贡献。几十年后，人们认识到微生物群中与疾病相关的变化，即生态失调，对黏膜内的能量获取提出了过高要求，尤其是在炎症活跃期。在此，我们从饥饿肠道假说提出的原始角度回顾黏膜健康与疾病中的组织能量学主题。
