Dietary riboflavin deficiency induces ariboflavinosis and esophageal epithelial atrophy in association with modification of gut microbiota in rats
Dietary riboflavin deficiency induces ariboflavinosis and esophageal epithelial atrophy in association with modification of gut microbiota in rats
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DOI：
10.1007/s00394-020-02283-4
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发表时间：
2020-05-26
影响因子：
5
通讯作者：
Xu, Li-Yan
中科院分区：
文献类型：
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作者：
Pan, Feng;Zhang, Ling-Li;Xu, Li-Yan
目的核黄素缺乏症是一种常见的营养缺乏性疾病。本研究旨在探讨核黄素缺乏对重要内脏器官的影响及其可能机制。方法实验一，雄性F344大鼠随机分为R-6（正常核黄素，6 mg/kg）组和R-0（核黄素缺乏，0 mg/kg）组。实验2大鼠分为R-6、R-0.6（0.6 mg/kg）和R-0.06（0.06 mg/kg）组。实验3大鼠被分配到R（6）和R-0 -> R-6（核黄素补充）组。根据16 S rRNA基因测序分析细菌群落。结果核黄素缺乏组大鼠出现核黄素中毒（R（0.06）46.7%; R（0）72%）和食管上皮萎缩（R（0.06）40%; R（0）44%），而R（6）组无明显症状（P < 0.001）。食管上皮萎缩与核黄素中毒同时发生（R（0.06）66.7%; R（0）63.6%）或单独发生（R（0.06）33.3%; R（0）36.4%）。食道是最脆弱的内脏器官。核黄素缺乏后补充（R-0 -> R-6）对核黄素缺乏症（83.3%vs.0%，P < 0.001）和食管上皮萎缩（66.7%vs.20%，P = 0.17）的治疗有效。核黄素缺乏调节肠道微生物群组成。几个关键菌属（Romboutsia、Turicillum和Clostridiumsensustricto 1）与核黄素中毒和食管上皮萎缩密切相关（P < 0.01或P < 0.05）。其潜在机制是肠道菌群影响机体对外源性物质的生物降解和代谢，以及基因组的不稳定性。结论核黄素缺乏通过调节肠道菌群引起核黄素缺乏症和食管上皮萎缩，为核黄素缺乏症和食管病变提供了新的见解。
Purpose Riboflavin deficiency causes ariboflavinosis, a common nutritional deficiency disease. The purpose of this study is to investigate the effects of riboflavin deficiency on the important internal organs and its potential mechanisms. Methods Experiment 1, male F344 rats were randomly assigned to R-6(normal riboflavin, 6 mg/kg) and R-0(riboflavin-deficient, 0 mg/kg) groups. Experiment 2 rats were assigned to R-6, R-0.6(0.6 mg/kg) and R-0.06(0.06 mg/kg) groups. Experiment 3 rats were assigned to R(6)and R-0 -> R-6(riboflavin replenishment) groups. Bacterial communities were analyzed based on 16S rRNA gene sequencing. Results Riboflavin deficiency induced ariboflavinosis (R(0.06)46.7%; R(0)72%) and esophageal epithelial atrophy (R(0.06)40%; R(0)44%) in rats, while the R(6)group did not display symptoms (P < 0.001, respectively). Esophageal epithelial atrophy occurred simultaneously (R(0.06)66.7%; R(0)63.6%) with ariboflavinosis or appeared alone (R(0.06)33.3%; R(0)36.4%). Esophagus is the most vulnerable internal organ. Riboflavin deficiency followed by replenishment (R-0 -> R-6) was effective in treating ariboflavinosis (83.3% vs. 0%,P < 0.001) and esophageal epithelial atrophy (66.7% vs. 20%,P = 0.17). Riboflavin deficiency modulated gut microbiota composition. The several key genera (Romboutsia,TuricibacterandClostridiumsensu stricto1) were strongly correlated with ariboflavinosis and esophageal epithelial atrophy (P < 0.01 orP < 0.05). The potential mechanism is that gut microbiota affects body's xenobiotic biodegradation and metabolism, and genomic instability. Conclusions Riboflavin deficiency induces ariboflavinosis and esophageal epithelial atrophy by modulating the gut microbiota, and offers new Queryinsight into riboflavin deficiency and esophageal lesions.