Dietary fructooligosaccharides increase intestinal permeability in rats
Dietary fructooligosaccharides increase intestinal permeability in rats
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DOI：
10.1093/jn/135.4.837
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发表时间：
2005-04-01
影响因子：
4.2
通讯作者：
Van der Meer, R
中科院分区：
文献类型：
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作者：
Ten Bruggencate, SJM;Bovee-Oudenhoven, IMJ;Van der Meer, R
我们之前表明，低聚果糖（FOS）会降低大鼠对沙门氏菌感染的抵抗力。然而，造成这种效应的机制尚不清楚。因此，我们研究了肠炎沙门氏菌感染前后膳食低聚果糖是否会影响肠道通透性。雄性威斯塔大鼠被喂食有限数量的模仿西方人类饮食成分的纯化饮食。饮食中补充了 60 g/kg 纤维素（对照）或 60 g/kg FOS 以及 4 mmol/kg 肠道通透性标记物铬 EDTA (CrEDTA)（n = 8 或 10）。经过2周的适应期后，大鼠经口感染108个菌落形成单位（cfu）的肠炎沙门氏菌。采用荧光法测量肠内容物和粘膜中的粘蛋白浓度，作为粘膜刺激的标志。通过测量尿 CrEDTA 排泄量来确定肠渗透性。通过分析尿液一氧化氮代谢物随时间的变化来量化沙门氏菌的易位。感染前，低聚果糖增加了盲肠和结肠中的粘膜乳酸杆菌和肠杆菌，但回肠中却没有增加。然而，低聚果糖增加了粪便水的细胞毒性和肠道通透性。此外，低聚果糖增加了粪便粘蛋白排泄以及盲肠和结肠内容物以及感染前盲肠粘膜中的粘蛋白浓度。感染后，与对照组相比，FOS 组的粘蛋白排泄和肠道通透性进一步增加。此外，低聚果糖增加了沙门氏菌向肠外部位的易位。因此，低聚果糖会损害大鼠的肠道屏障，肠道通透性较高就表明了这一点。这些结果是否可以推断到人类身上还需要进一步研究。
We showed previously that fructooligosaccharides (FOS) decrease the resistance to salmonella infection in rats. However, the mechanism responsible for this effect is unclear. Therefore, we examined whether dietary FOS affects intestinal permeability before and after infection with Salmonella enterica serovar Enteritidis. Male Wistar rats were fed restricted quantities of a purified diet that mimicked the composition of a Western human diet. The diet was supplemented with 60 g/kg cellulose (control) or 60 g/kg FOS and with 4 mmol/kg of the intestinal permeability marker chromium EDTA (CrEDTA) (n = 8 or 10). After an adaptation period of 2 wk, rats were orally infected with 108 colony-forming units (cfu) of S. enteritidis. Mucin concentrations in intestinal contents and mucosa were measured fluori metrically, as markers of mucosal irritation. Intestinal permeability was determined by measuring urinary CrEDTA excretion. Translocation of salmonella was quantified by analysis of urinary nitric oxide metabolites with time. Before infection, FOS increased mucosal lactobacilli and enterobacteria in cecum and colon, but not in the ileum. However, FOS increased cytotoxicity of fecal water and intestinal permeability. Moreover, FOS increased fecal mucin excretion and mucin concentrations in cecal and colonic contents, and in cecal mucosa before infection. After infection, mucin excretion and intestinal permeability in the FOS groups increased even further in contrast to the control group. In addition, FOS increased translocation of salmonella to extraintestinal sites. Thus, FOS impairs the intestinal barrier in rats, as indicated by higher intestinal permeability. Whether these results can be extrapolated to humans requires further investigation.