Research Institute of Chinese Medical Clinical Foundation and Immunology, School of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, China; Key Laboratory of Chinese Medicine Rheumatology of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou 310053, China.
Department of Epidemiology, School of Public Health, Zhejiang Chinese Medical University, Hangzhou 310053, China.
Ecotoxicol Environ Saf. 2024 Aug;281:116604. doi: 10.1016/j.ecoenv.2024.116604. Epub 2024 Jun 18.
Irritable bowel syndrome (IBS) patients exhibit significantly lower levels of serum selenium (Se) compared to healthy controls. This study integrates a prospective cohort analysis and animal experiments to investigate Se deficiency as a potential risk factor for IBS. Using data from the UK Biobank, a longitudinal analysis was conducted to explore the associations between dietary Se intake and the risk of incident IBS. In animal study, C57BL/6 mice were fed diets with normal (0.2 ppm) or low (0.02 ppm) Se levels to assess the impacts of Se deficiency on IBS symptoms. Furthermore, we performed 16 S rRNA sequencing, untargeted colonic fecal metabolomics analysis, and colon transcriptome profiling to uncover the regulatory mechanisms underlying Se deficiency-induced IBS. The analysis of UK Biobank data revealed a significant correlation between low dietary Se levels and an increased incidence of IBS. In the experimental study, a low Se diet induced IBS symptoms, evidenced by elevated abdominal withdrawal reflex scores, colon inflammation, and severe pathological damage to the colon. Additionally, the low Se diet caused disturbances in gut microbiota, characterized by an increase in Faecalibaculum and Helicobacter, and a decrease in Bifidobacterium and Akkermansia. Combined colonic fecal metabolomics and colon transcriptome analysis indicated that Se deficiency might trigger IBS through disruptions in pathways related to "bile excretion", "steroid hormone biosynthesis", "arachidonic acid metabolism", and "drug metabolism-cytochrome P450". These findings underscore the significant adverse effects of Se deficiency on IBS and suggest that Se supplementation should be considered for IBS patients.
肠易激综合征（IBS）患者的血清硒（Se）水平明显低于健康对照组。本研究通过前瞻性队列分析和动物实验，将硒缺乏作为 IBS 的潜在危险因素进行综合研究。利用英国生物银行（UK Biobank）的数据进行纵向分析，探讨膳食 Se 摄入与 IBS 发病风险之间的关系。在动物研究中，用正常（0.2ppm）或低（0.02ppm）Se 水平的饮食喂养 C57BL/6 小鼠，以评估 Se 缺乏对 IBS 症状的影响。此外，我们进行了 16S rRNA 测序、非靶向性结肠粪便代谢组学分析和结肠转录组谱分析，以揭示 Se 缺乏诱导 IBS 的调控机制。对 UK Biobank 数据分析显示，低膳食 Se 水平与 IBS 发病率增加显著相关。在实验研究中，低 Se 饮食诱导 IBS 症状，表现为腹壁退缩反射评分升高、结肠炎症和结肠严重病理损伤。此外，低 Se 饮食导致肠道微生物群失调，表现为 Faecalibaculum 和 Helicobacter 增加，Bifidobacterium 和 Akkermansia 减少。结肠粪便代谢组学和结肠转录组学联合分析表明，Se 缺乏可能通过破坏与“胆汁排泄”、“类固醇激素生物合成”、“花生四烯酸代谢”和“药物代谢-细胞色素 P450”相关的途径引发 IBS。这些发现强调了 Se 缺乏对 IBS 的显著不良影响，并提示 IBS 患者应考虑补充 Se。
