背景:非乳糜泻面筋/小麦敏感性(NCGWS)的个体在无麸质饮食后经历胃肠道症状的改善。尽管以前的结果表明低聚果糖(FOS),一种短链果聚糖,在自我报告的NCGWS患者中,比麸质更容易诱发症状,潜在的机制尚未解决。
方法:因此,我们的主要目标是调查FOS-果聚糖和麸质是否影响粪便微生物群的组成和多样性(16SrRNA基因测序),微生物发酵的粪便代谢产物(短链脂肪酸[SCFA];火焰离子化检测器气相色谱法),和肠道炎症的粪便生物标志物(中性粒细胞明胶酶相关脂质运载蛋白,也称为脂质运载蛋白2,NGAL/LCN2;ELISA)。在随机双盲安慰剂对照交叉研究中,59名自我报告为NCGWS的参与者接受了三种不同的7天饮食挑战与麸质(5.7克/天),FOS-果聚糖(2.1克/天),和安慰剂分别(三个时期,六个挑战序列)。
结果:某些细菌类群的相对丰度受到饮食挑战的不同影响。在FOS-果聚糖挑战之后,镰刀菌增加,而真细菌(E.)共生前列腺素组,anaerotruncus,未知的反刍动物科属减少。谷蛋白攻击的主要特征是嗜木聚糖真杆菌组的丰度增加。然而,细菌多样性(α-多样性)没有发现差异,总体细菌群落结构(β-多样性),粪便代谢物(SCFA),或NGAL/LCN2。此外,响应FOS-果聚糖的胃肠道症状通常与肠道细菌群落的实质性变化无关。然而,在FOS-果聚糖激发后,E.共生甾体多糖组的减少与胃肠道疼痛增加相关.最后,相关分析显示,FOS-果聚糖和麸质攻击后胃肠道症状的变化与基线时不同的细菌丰度有关.
结论:结论:而在NCGWS患者中,FOS-果聚糖比麸质引起更多的胃肠道症状,我们没有发现粪便微生物群组成和功能的实质性变化可以解释本研究中的这些差异.然而,我们的结果表明,基线细菌组成/功能的个体差异可能会影响对FOS-果聚糖和谷蛋白的胃肠道症状反应.此外,E.共骨多糖组的变化,这与症状增加有关,提示在未来研究饮食治疗对胃肠道症状影响的试验中,应注意这些细菌.
背景:Clinicaltrials.gov作为NCT02464150。
BACKGROUND: Individuals with non-celiac gluten/wheat sensitivity (NCGWS) experience improvement in gastrointestinal symptoms following a gluten-free diet. Although previous results have indicated that fructo-oligosaccharides (FOS), a type of short-chain fructans, were more likely to induce symptoms than gluten in self-reported NCGWS patients, the underlying mechanisms are unresolved.
METHODS: Our main objective was therefore to investigate whether FOS-fructans and gluten affect the composition and diversity of the faecal microbiota (16S rRNA gene sequencing), faecal metabolites of microbial fermentation (short-chain fatty acids [SCFA]; gas chromatography with flame ionization detector), and a faecal biomarker of gut inflammation (neutrophil gelatinase-associated lipocalin, also known as lipocalin 2, NGAL/LCN2; ELISA). In the randomised double-blind placebo-controlled crossover
study, 59 participants with self-reported NCGWS underwent three different 7-day diet challenges with gluten (5.7 g/day), FOS-fructans (2.1 g/day), and placebo separately (three periods, six challenge sequences).
RESULTS: The relative abundances of certain bacterial taxa were affected differently by the diet challenges. After the FOS-fructan challenge, Fusicatenibacter increased, while Eubacterium (E.) coprostanoligenes group, Anaerotruncus, and unknown Ruminococcaceae genera decreased. The gluten challenge was primarily characterized by increased abundance of Eubacterium xylanophilum group. However, no differences were found for bacterial diversity (α-diversity), overall bacterial community structure (β-diversity), faecal metabolites (SCFA), or NGAL/LCN2. Furthermore, gastrointestinal symptoms in response to FOS-fructans were generally not linked to substantial shifts in the gut bacterial community. However, the reduction in E. coprostanoligenes group following the FOS-fructan challenge was associated with increased gastrointestinal pain. Finally, correlation analysis revealed that changes in gastrointestinal symptoms following the FOS-fructan and gluten challenges were linked to varying bacterial abundances at baseline.
CONCLUSIONS: In conclusion, while FOS-fructans induced more gastrointestinal symptoms than gluten in the NCGWS patients, we did not find that substantial shifts in the composition nor function of the faecal microbiota could explain these differences in the current
study. However, our results indicate that individual variations in baseline bacterial composition/function may influence the gastrointestinal symptom response to both FOS-fructans and gluten. Additionally, the change in E. coprostanoligenes group, which was associated with increased symptoms, implies that attention should be given to these bacteria in future trials investigating the impact of dietary treatments on gastrointestinal symptoms.
BACKGROUND: Clinicaltrials.gov as NCT02464150.