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Alterations in gut motility and visceral hypersensitivity are two majorfeatures of irritable bowel syndrome (IBS). The aim of this study was to investigatethe roles of glucagon-like peptide-1 (GLP-1) in the pathogenesis of experimentalIBS. Rat models of constipation-predominant IBS (IBS-C) and diarrhea-predominantIBS (IBS-D) were established. Fecal water content and behavioral responses tocolorectal distention (CRD), using electromyography (EMG), were measured. Theexpression of glucagon-like peptide-1 receptor (GLP-1R) in the colon was detectedby immunohistochemistry, and the serum concentration of GLP-1 was measured byELISA assay. The movement of circular and longitudinal colonic muscle was detectedusing an organ bath recording technique. Compared to controls, the fecal watercontents were lower in the IBS-C group, while they were higher in the IBS-D group(P&lt;0.05). EMG response to CRD in the experimental IBS groups was increasedcompared with their respective controls (P&lt;0.05). GLP-1R was localized in themucosa layer, circular muscle and myenteric nerve plexus of the colon. Notably,the expression of GLP-1R in the IBS-C group was higher, but in the IBS-D group,it was lower compared with controls. The serum levels of GLP-1 in the IBS-C groupwere higher compared to those in the IBS-D group (P&lt;0.05). In addition, administrationof exogenous GLP-1 and exendin-4 inhibited colonic circular muscle contraction,particularly in the IBS-C group, while there was no significant effect on longitudinalmuscle contraction. In conclusion, these results indicated that GLP-1 and GLP-1Rare implicated in the pathogenesis of IBS-C and IBS-D.

Role of glucagon-like peptide-1 in the pathogenesis of experimental irritable bowel syndrome rat models