APC Microbiome Institute, University College Cork, Cork, Ireland.
School of Microbiology, University College Cork, Cork, Ireland.
J Crohns Colitis. 2018 Jan 24;12(2):204-216. doi: 10.1093/ecco-jcc/jjx137.
BACKGROUND AND AIMS: Alterations in short chain fatty acid metabolism, particularly butyrate, have been reported in inflammatory bowel disease, but results have been conflicting because of small study numbers and failure to distinguish disease type, activity or other variables such as diet. We performed a comparative assessment of the capacity of the microbiota for butyrate synthesis, by quantifying butyryl-CoA:acetate CoA-transferase [BCoAT] gene content in stool from patients with Crohn's disease [CD; n = 71], ulcerative colitis [UC; n = 58] and controls [n = 75], and determined whether it was related to active vs inactive inflammation, microbial diversity, and composition and/or dietary habits. METHODS: BCoAT gene content was quantified by quantitative polymerase chain reaction [qPCR]. Disease activity was assessed clinically and faecal calprotectin concentration measured. Microbial composition was determined by sequencing 16S rRNA gene. Dietary data were collected using an established food frequency questionnaire. RESULTS: Reduced butyrate-synthetic capacity was found in patients with active and inactive CD [p < 0.001 and p < 0.01, respectively], but only in active UC [p < 0.05]. In CD, low BCoAT gene content was associated with ileal location, stenotic behaviour, increased inflammation, lower microbial diversity, greater microbiota compositional change, and decreased butyrogenic taxa. Reduced BCoAT gene content in patients with CD was linked with a different regimen characterised by lower dietary fibre. CONCLUSIONS: Reduced butyrate-synthetic capacity of the microbiota is more evident in CD than UC and may relate to reduced fibre intake. The results suggest that simple replacement of butyrate per se may be therapeutically inadequate, whereas manipulation of microbial synthesis, perhaps by dietary means, may be more appropriate.
背景和目的:短链脂肪酸代谢的改变,特别是丁酸盐,在炎症性肠病中已有报道,但由于研究数量较少且未能区分疾病类型、活动度或其他变量(如饮食),结果存在冲突。我们通过定量检测粪便中丁酰辅酶 A:乙酰辅酶 A 转移酶(BCoAT)基因含量,对微生物合成丁酸盐的能力进行了比较评估,该基因含量来自克罗恩病(CD;n = 71)、溃疡性结肠炎(UC;n = 58)和对照组(n = 75)患者。并确定其是否与活跃与不活跃的炎症、微生物多样性、组成和/或饮食习惯有关。
方法:通过定量聚合酶链反应(qPCR)定量检测 BCoAT 基因含量。临床评估疾病活动度,测定粪便钙卫蛋白浓度。通过 16S rRNA 基因测序确定微生物组成。使用既定的食物频率问卷收集饮食数据。
结果:发现活跃和不活跃的 CD 患者的丁酸盐合成能力降低(p < 0.001 和 p < 0.01),但仅在活跃的 UC 患者中降低(p < 0.05)。在 CD 中,低 BCoAT 基因含量与回肠部位、狭窄行为、炎症增加、微生物多样性降低、微生物组成变化更大以及产丁酸菌减少有关。CD 患者 BCoAT 基因含量降低与膳食纤维摄入较低的不同饮食方案有关。
结论:与 UC 相比,CD 患者的微生物丁酸盐合成能力降低更为明显,可能与膳食纤维摄入减少有关。结果表明,简单地替代丁酸盐本身可能在治疗上是不够的,而通过饮食等方式对微生物合成的干预可能更为恰当。
Gut. 2017-5
World J Gastroenterol. 2018-4-7
Cell Mol Gastroenterol Hepatol. 2020
Nat Rev Microbiol. 2025-5-13
Pharmaceuticals (Basel). 2024-3-7