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Glucagonlike peptide-1 (GLP-1) participation in ileal brake induced by intraluminal peptones in rat
The aim of this study was to determine the mechanisms implicated in the gastrointestinal inhibition induced by ovoalbumin hydrolysate infused intraluminally. We studied the site of action, the possible implication of GLP-1, and the nervous mechanisms involved. We prepared anesthetized Sprague-Dawley...
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Published in: | Digestive diseases and sciences 1999-02, Vol.44 (2), p.322-329 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | The aim of this study was to determine the mechanisms implicated in the gastrointestinal inhibition induced by ovoalbumin hydrolysate infused intraluminally. We studied the site of action, the possible implication of GLP-1, and the nervous mechanisms involved. We prepared anesthetized Sprague-Dawley rats with strain gauges in the antrum, duodenum, and proximal jejunum and a catheter in the duodenum or ileum for peptone infusion. Both intraduodenal (N = 6) and intraileal (N = 5) infusion of ovoalbumin hydrolysate induced inhibition of spontaneous motor activity in the antrum, duodenum, and proximal jejunum. Duodenal inhibition induced by intraduodenal (N = 6) or intraileal (N = 6) infusion of ovoalbumin hydrolysate was reversed by intraarterial infusion of GLP-1 receptor antagonist, exendin (9-39) (3 x 10(-8) mol/kg/40 min). Finally, a combination of the adrenergic blockers phentolamine and propranolol (1 mg/kg, each; N = 7) completely blocked inhibitory gastrointestinal motor actions caused by intraduodenal infusion of ovoalbumin hydrolysate. This study demonstrates that peptone, intraluminally infused, participates in the regulation of gastrointestinal motility through stimulation of adrenergic pathways in anaesthetized rats. Moreover, these effects are partly mediated by GLP-1 secretion. The ileum seems to be the site of action, indicating a role of GLP-1 on the ileal break mechanism. |
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ISSN: | 0163-2116 1573-2568 |
DOI: | 10.1023/A:1026654417697 |