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Published on: January 5, 2017
Stress-induced intestinal barrier dysfunction is exacerbated during diet-induced obesity
Wafa Bahlouli1, Jonathan Breton1, Mauranne Lelouard1
1Normandie University, UNIROUEN, INSERM UMR 1073 "Nutrition, inflammation and gut-brain axis", 76183 Rouen, France; Institute of Research and Innovation in Biomedicine (IRIB), UNIROUEN, 76183 Rouen, France.
Stress exacerbates intestinal barrier dysfunction in diet-induced obesity, independent of leptin or gut microbiota. This finding offers new insights into the obesity and irritable bowel syndrome (IBS) link.
Area of Science:
- Gastroenterology
- Endocrinology
- Microbiology
Background:
- Obesity and irritable bowel syndrome (IBS) are significant public health concerns.
- Increased IBS prevalence is noted in obese individuals, but mechanisms are unclear.
- Shared pathways include gut dysbiosis, hyperpermeability, and inflammation.
Purpose of the Study:
- To investigate the relationship between obesity and IBS using animal models.
- To explore the impact of stress on intestinal barrier function in diet-induced obesity.
Main Methods:
- Male C57Bl/6 mice were fed a high-fat diet (HFD) for 12 weeks, followed by water avoidance stress (WAS).
- Evaluated intestinal permeability, plasma corticosterone, and effects of metformin and microbiota transplantation.
- Compared responses in HFD mice, ob/ob mice, and leptin-treated mice.
Main Results:
- HFD mice under WAS showed increased intestinal permeability and corticosterone compared to non-obese mice.
- Metformin partially restored colonic permeability in unstressed HFD mice but failed in stressed HFD mice.
- Leptin and microbiota transplantation did not replicate the stress-induced barrier dysfunction in HFD mice.
Conclusions:
- Stress significantly worsens intestinal barrier dysfunction in diet-induced obese mice.
- This effect appears independent of leptin, glycemic control, and gut microbiota composition.
- Further research is needed to confirm findings and explore dietary influences.
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