丁酸盐
炎症
紧密连接
脂多糖
肠道菌群
内科学
丁酸钠
内分泌学
回肠
一元羧酸盐转运体
饮食性肥胖
粘蛋白2
粘蛋白
促炎细胞因子
运输机
生物
免疫学
医学
肥胖
生物化学
基因表达
胰岛素抵抗
基因
发酵
作者
Laura Benvenuti,Vanessa D’Antongiovanni,Carolina Pellegrini,Matteo Fornai,Nunzia Bernardini,Chiara Ippolito,Cristina Segnani,Clelia Di Salvo,Rocchina Colucci,Alma Martelli,Lorenzo Flori,Vincenzo Calderone,Gianfranca Carta,Emilia Ghelardi,Marco Calvigioni,Adelaide Panattoni,Raffaella Coppolecchia,Achille Arini,Luca Antonioli
标识
DOI:10.1002/mnfr.202200442
摘要
Scope Modifications in intestinal microbiota and its metabolites, the short‐chain fatty acids (SCFA) are main factors altering intestinal epithelial barrier integrity and eliciting the onset of a meta‐inflammation observed in obesity. The present study is aimed at evaluating the efficacy of Enterococcus faecium (SF68) administration in counteracting the impairment of gut barrier and enteric inflammation in a model of diet‐induced obesity, characterizing the molecular mechanisms underlying such beneficial effects. Methods and Results Male C57BL/6J mice, fed with standard diet (SD) or high‐fat diet (HFD), are treated with SF68 (10 8 CFU day −1 ). After 8 weeks, plasma interleukin (IL)‐1β and lipopolysaccharide binding protein (LBP) are measured, analysis of fecal microbiota composition and butyrate content as well as intestinal malondialdehyde, myeloperoxidase, mucins, tight junction protein, and butyrate transporter expression are investigated. After 8 weeks, SF68 administration counteracts the body weight gain in HFD mice, reducing plasma IL‐1β and LBP. In parallel, SF68 treatment acts against the intestinal inflammation in HFD‐fed animals and improves the intestinal barrier integrity and functionality in obese mice via the increase in tight junction protein and intestinal butyrate transporter (sodium‐coupled monocarboxylate transporter 1 ) expression. Conclusions Supplementation with SF68 reduces intestinal inflammation and reinforces the enteric epithelial barrier in obese mice, improving the transport and utilization of butyrate.
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