Obesity and irritable bowel syndrome (IBS) are two major public health issues. Interestingly previous data report a marked increase of IBS prevalence in morbid obese subjects compared with non-obese subjects but underlying mechanisms remain unknown. Obesity and IBS share common intestinal pathophysiological mechanisms such as gut dysbiosis, intestinal hyperpermeability and low-grade inflammatory response. We thus aimed to evaluate the link between obesity and IBS using different animal models. Male C57Bl/6 mice received high fat diet (HFD) for 12 weeks and were then submitted to water avoidance stress (WAS). In response to WAS, HFD mice exhibited higher intestinal permeability and plasma corticosterone concentration than non-obese mice. We were not able to reproduce a similar response both in ob/ob mice and in leptin-treated non-obese mice. In addition, metformin, a hypoglycemic agent, limited fasting glycaemia both in unstressed and WAS diet-induced obese mice but only partially restored colonic permeability in unstressed HFD mice. Metformin failed to improve intestinal permeability in WAS HFD mice. Finally, cecal microbiota transplantation from HFD mice in antibiotics-treated recipient mice did not reproduce the effects observed in stressed HFD mice. In conclusion, stress induced a more marked intestinal barrier dysfunction in diet-induced obese mice compared with non-obese mice that seems to be independent of leptin, glycaemia and gut microbiota. These data should be further confirmed and the role of the dietary composition should be studied.

肥胖和肠易激综合症（IBS）是两个主要的公共卫生问题。有趣的是，先前的数据报道病态肥胖受试者的IBS患病率较非肥胖受试者显着增加，但其潜在机制仍不清楚。肥胖和IBS有共同的肠道病理生理机制，例如肠道营养不良，肠道通透性过高和低度炎症反应。因此，我们旨在使用不同的动物模型评估肥胖与IBS之间的联系。雄性C57Bl / 6小鼠接受高脂饮食（HFD）持续12周，然后接受避水胁迫（WAS）。响应WAS，HFD小鼠比非肥胖小鼠表现出更高的肠通透性和血浆皮质酮浓度。我们无法在ob / ob小鼠和瘦素治疗的非肥胖小鼠中均产生类似的反应。此外，二甲双胍（一种降血糖药）在未应激和WAS饮食诱导的肥胖小鼠中均限制了空腹血糖，但在未应激的HFD小鼠中仅部分恢复了结肠通透性。二甲双胍未能改善WAS HFD小鼠的肠通透性。最后，在接受抗生素治疗的受体小鼠中，从HFD小鼠中盲肠进行微生物菌群移植并没有重现在紧张的HFD小鼠中观察到的效果。总之，与非肥胖小鼠相比，饮食诱导的肥胖小鼠中应激引起的肠道屏障功能异常更为明显，而肥胖小鼠似乎与瘦素，血糖和肠道菌群无关。这些数据应进一步确认，并应研究饮食组成的作用。在未应激和WAS饮食诱导的肥胖小鼠中均限制了空腹血糖，但在未应激HFD小鼠中仅部分恢复了结肠通透性。二甲双胍未能改善WAS HFD小鼠的肠通透性。最后，在接受抗生素治疗的受体小鼠中从HFD小鼠进行盲肠微生物菌群移植不能重现在紧张的HFD小鼠中观察到的效果。总之，与非肥胖小鼠相比，饮食诱导的肥胖小鼠中应激引起的肠道屏障功能障碍更为明显，这似乎与瘦素，血糖和肠道菌群无关。这些数据应进一步确认，并应研究饮食组成的作用。在未应激和WAS饮食诱导的肥胖小鼠中均限制了空腹血糖，但在未应激HFD小鼠中仅部分恢复了结肠通透性。二甲双胍未能改善WAS HFD小鼠的肠通透性。最后，在接受抗生素治疗的受体小鼠中从HFD小鼠进行盲肠微生物菌群移植不能重现在紧张的HFD小鼠中观察到的效果。总之，与非肥胖小鼠相比，饮食诱导的肥胖小鼠中应激引起的肠道屏障功能异常更为明显，而肥胖小鼠似乎与瘦素，血糖和肠道菌群无关。这些数据应进一步确认，并应研究饮食组成的作用。在接受抗生素治疗的受体小鼠中，从HFD小鼠进行盲肠微生物群移植不能重现在压力高的HFD小鼠中观察到的效果。总之，与非肥胖小鼠相比，饮食诱导的肥胖小鼠中应激引起的肠道屏障功能障碍更为明显，这似乎与瘦素，血糖和肠道菌群无关。这些数据应进一步确认，并应研究饮食组成的作用。在接受抗生素治疗的受体小鼠中，从HFD小鼠进行盲肠微生物群移植不能重现在压力高的HFD小鼠中观察到的效果。总之，与非肥胖小鼠相比，饮食诱导的肥胖小鼠中应激引起的肠道屏障功能异常更为明显，而肥胖小鼠似乎与瘦素，血糖和肠道菌群无关。这些数据应进一步确认，并应研究饮食组成的作用。