GLUCAGON-LIKE PEPTIDE-1 7-36-AMIDE AND PEPTIDE-YY FROM THE L-CELL OF THE ILEAL-MUCOSA ARE POTENT INHIBITORS OF VAGALLY INDUCED GASTRIC-ACIDSECRETION IN MAN

Citation
A. Wettergren et al., GLUCAGON-LIKE PEPTIDE-1 7-36-AMIDE AND PEPTIDE-YY FROM THE L-CELL OF THE ILEAL-MUCOSA ARE POTENT INHIBITORS OF VAGALLY INDUCED GASTRIC-ACIDSECRETION IN MAN, Scandinavian journal of gastroenterology, 29(6), 1994, pp. 501-505
Citations number
28
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
00365521
Volume
29
Issue
6
Year of publication
1994
Pages
501 - 505
Database
ISI
SICI code
0036-5521(1994)29:6<501:GP7APF>2.0.ZU;2-2
Abstract
Background: Glucagon-like peptide (GLP-1) 7-36 amide and peptide YY (P YY) from the L-cell of the ileal mucosa are potent inhibitors of gastr ic acid secretion in man. It is not clear, however, by which mechanism (s) they inhibit acid secretion. In dogs the inhibitory effect of PYY on acid secretion may be mediated mainly through neural pathways. The mechanism of action of GLP-1 might be similar. The aim of the present study was to examine the effects of GLP-1 might be similar. The aim of the present study was to examine the effects of GLP-1 and PW on the v agally induced gastric acid secretion in man. Methods: A modified sham feeding technique, chew and spit, was used. Six healthy volunteers we re randomly assigned to receive intravenous infusion of saline, GLP-1 (41 pmol/kg/h), or peptide W (50 pmol/kg/h). Results: The infusion of GLP-1 and PW resulted in plasma concentrations of 60 +/- 9 pmol/l and 84 +/- 11 pmol/l, respectively. GLP-1 and PYY both significantly inhib ited the integrated acid output by 67 +/- 6% and 68 +/- 9%, respective ly, compared with the integrated outputs in a control experiment with saline infusion. Serum gastrin and plasma somatostatin concentrations remained unchanged during saline, GLP-1, and PW infusions. Conclusions : GLP-1 and PYY are both potent inhibitors of the cephalic phase of ac id secretion, indicating that at least part of the inhibitory effect o f GLP-1 and PW in man is mediated through neural pathways. Furthermore , the inhibitory effect seems to be independent of circulating concent rations of gastrin and somatostatin.