title: Role of glucagon-like peptide-1 in the pathogenesis of experimental             irritable bowel syndrome rat models.
abstract: Alterations in gut motility and visceral hypersensitivity are two major             features of irritable bowel syndrome (IBS). The aim of this study was to investigate             the roles of glucagon-like peptide-1 (GLP-1) in the pathogenesis of experimental             IBS. Rat models of constipation-predominant IBS (IBS-C) and diarrhea-predominant             IBS (IBS-D) were established. Fecal water content and behavioral responses to             colorectal distention (CRD), using electromyography (EMG), were measured. The             expression of glucagon-like peptide-1 receptor (GLP-1R) in the colon was detected             by immunohistochemistry, and the serum concentration of GLP-1 was measured by             ELISA assay. The movement of circular and longitudinal colonic muscle was detected             using an organ bath recording technique. Compared to controls, the fecal water             contents were lower in the IBS-C group, while they were higher in the IBS-D group             (P<0.05). EMG response to CRD in the experimental IBS groups was increased             compared with their respective controls (P<0.05). GLP-1R was localized in the             mucosa 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 group             were higher compared to those in the IBS-D group (P<0.05). In addition, administration             of exogenous GLP-1 and exendin-4 inhibited colonic circular muscle contraction,             particularly in the IBS-C group, while there was no significant effect on longitudinal             muscle contraction. In conclusion, these results indicated that GLP-1 and GLP-1R             are implicated in the pathogenesis of IBS-C and IBS-D.
authors: Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, PR China.
authors: Yan
authors: Y
authors: Chen
authors: Zhengyang
authors: Z
authors: Li
authors: Yan
authors: Y
authors: Yang
authors: Lin
authors: L
authors: Lin
authors: Hongjie
authors: H
authors: Zhang
mesh_terms: D000818:Animals; D003106:Colon / Q000502:physiology; D003248:Constipation; D003967:Diarrhea; D004195:Disease Models, Animal; D000077270:Exenatide; D005243:Feces / Q000737:chemistry; D052216:Glucagon-Like Peptide 1 / Q000378:metabolism* / Q000494:pharmacology; D000067757:Glucagon-Like Peptide-1 Receptor; D043183:Irritable Bowel Syndrome / Q000378:metabolism*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D010455:Peptides / Q000494:pharmacology; D010528:Peristalsis; D051381:Rats; D017207:Rats, Sprague-Dawley; D018027:Receptors, Glucagon / Q000378:metabolism*; D014688:Venoms / Q000494:pharmacology; D014867:Water / Q000737:chemistry
chemical_list: C000593835:Glp1r protein, rat; D000067757:Glucagon-Like Peptide-1 Receptor; D010455:Peptides; D018027:Receptors, Glucagon; D014688:Venoms; D014867:Water; D052216:Glucagon-Like Peptide 1; D000077270:Exenatide