Glucagon-like peptide (GLP-1) is involved in the central modulation of fecal output in rats


Gulpinar M. A. , Bozkurt A., Coskun T., Ulusoy N., Yegen B.

AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, vol.278, no.6, 2000 (Journal Indexed in SCI) identifier identifier

  • Publication Type: Article / Article
  • Volume: 278 Issue: 6
  • Publication Date: 2000
  • Title of Journal : AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
  • Keywords: glucagon-like peptide 1, exendin, astressin, CORTICOTROPIN-RELEASING FACTOR, COLONIC MOTOR ALTERATIONS, PARAVENTRICULAR NUCLEUS, EMOTIONAL-STRESS, RESTRAINT STRESS, BRAIN, EXPRESSION, CRF, RECEPTORS, MOTILITY

Abstract

In addition to its insulinotropic action, exogenously administered glucagon-like peptide (GLP-1) inhibits gastropancreatic motility and secretion via central pathways. The aims of the present study were to evaluate the effects of exogenous GLP-1-(7-36) amide on fecal output and to investigate the role of endogenous GLP-1 on stress-induced colonic activity. With the use of a stereotaxic instrument, adult male Sprague-Dawley rats weighing 200-250 g were fitted with stainless steel cerebroventricular guide cannulas under ketamine anesthesia. A group of rats were placed in Bollman-type cages to induce restraint stress. Fecal output monitored for 2 h was increased significantly by intracerebroventricular GLP-1 to 500, 1,000, and 3,000 pmol/rat (P < 0.05-0.01), whereas intraperitoneal GLP-1 had no effect. Intracerebroventricular administration of the GLP-1 receptor antagonist exendin-(9-39) (10 nmol/rat) reversed the increases induced by GLP-1 (500 pmol/rat; P < 0.01). Similar results were also observed with the injection of corticotropin-releasing factor receptor antagonist astressin (10 mu g/rat icv). The significant increase in fecal pellet output induced by restraint stress was also decreased by both intracerebroventricular exendin (10 nmol/rat) and astressin (10 mu g/rat; P < 0.01-0.001). These results suggest that GLP-1 participates in the central, but not peripheral, regulation of colonic motility via its own receptor and that GLP-1 is likely to be a candidate brain-gut peptide that acts as a physiological modulator of stress-induced colonic motility.