



How might altered sensitivity contribute to IBS? Can alterations in the gut's production of glucagon-like peptide-1 (GLP-1) contribute to the onset of IBS symptoms by affecting motility and satiety?
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- Are there any factors that can damage or affect the integrity of tight junctions? Can changes in the communication between the gut and the brain via the hypothalamic-pituitary-adrenal (HPA) axis contribute to the onset of IBS?
- How might altered sensitivity contribute to IBS? Can alterations in the gut's production of bradykinin contribute to the onset of IBS symptoms by affecting pain and inflammation?
- How might their dysregulation be involved in IBS? Can changes in the gut's response to macrophages contribute to the onset of IBS symptoms by affecting inflammation and immune regulation?
- How might their altered expression or function be involved in IBS? Can alterations in the gut's processing of bile salts by bacteria contribute to the onset of IBS symptoms like diarrhea?
- Are there specific dietary patterns high in lectins that have been associated with an increased risk of IBS? Can alterations in the metabolism of short-chain fatty acids (SCFAs) in the gut contribute to the onset of IBS?
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