CCK-1 and CCK-2 receptor agonism do not stimulate GLP-1 and neurotensin secretion in the isolated perfused rat small intestine or GLP-1 and PYY secretion in the rat colon.
Animals
Cholecystokinin
/ pharmacology
Colon
/ drug effects
Gastrins
/ pharmacology
Glucagon-Like Peptide 1
/ metabolism
Intestine, Small
/ drug effects
Male
Neurotensin
/ metabolism
Peptide YY
/ metabolism
Rats
Rats, Wistar
Receptor, Cholecystokinin B
/ agonists
Receptors, Cholecystokinin
/ agonists
Vasoactive Intestinal Peptide
/ pharmacology
CCK
GIP
GLP-1
PYY
VIP
bombesin
cholecystokinin
colon
ex vivo
gastrin
glucagon-like peptide-1
glucose-dependent insulinotropic polypeptide
hormones
isolated perfused colon
isolated perfused small intestine
neurotensin
peptide YY
rat
secretion
vasoactive intestinal peptide
Journal
Physiological reports
ISSN: 2051-817X
Titre abrégé: Physiol Rep
Pays: United States
ID NLM: 101607800
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
received:
03
11
2019
revised:
21
12
2019
accepted:
24
12
2019
entrez:
28
1
2020
pubmed:
28
1
2020
medline:
2
1
2021
Statut:
ppublish
Résumé
Gastrin and cholecystokinin (CCK) are hormones released from endocrine cells in the antral stomach (gastrin), the duodenum, and the jejunum (CCK). Recent reports, based on secretion experiments in an enteroendocrine cell line (NCI-H716) and gastrin receptor expression in proglucagon-expressing cells from the rat colon, suggested that gastrin could be a regulator of glucagon-like peptide-1 (GLP-1) secretion. To investigate these findings, we studied the acute effects of CCK-8 (a CCK1/CCK2 (gastrin) receptor agonist) and gastrin-17 (a CCK2(gastrin) receptor agonist) in robust ex vivo models: the isolated perfused rat small intestine and the isolated perfused rat colon. Small intestines from Wistar rats (n = 6), were perfused intraarterially over 80 min. During the perfusion, CCK (1 nmol/L) and gastrin (1 nmol/L) were infused over 10-min periods separated by washout/baseline periods. Colons from Wistar rats (n = 6) were perfused intraarterially over 100 min. During the perfusion, CCK (1 nmol/L), vasoactive intestinal peptide (VIP) (10 nmol/L), and glucose-dependent insulinotropic polypeptide (GIP) (1 nmol/L) were infused over 10-min periods separated by washout/baseline periods. In the perfused rat small intestines neither CCK nor gastrin stimulated the release of GLP-1 or neurotensin. In the perfused rat colon, neither CCK or VIP stimulated GLP-1 or peptide YY (PYY) release, but GIP stimulated both GLP-1 and PYY release. In both sets of experiments, bombesin, a gastrin-releasing peptide analog, served as a positive control. Our findings do not support the suggestion that gastrin or CCK participate in the acute regulation of intestinal GLP-1 secretion, but that GIP may play a role in the regulation of hormone secretion from the colon.
Identifiants
pubmed: 31984675
doi: 10.14814/phy2.14352
pmc: PMC6983481
doi:
Substances chimiques
Gastrins
0
Receptor, Cholecystokinin B
0
Receptors, Cholecystokinin
0
Peptide YY
106388-42-5
Vasoactive Intestinal Peptide
37221-79-7
Neurotensin
39379-15-2
Glucagon-Like Peptide 1
89750-14-1
Cholecystokinin
9011-97-6
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e14352Subventions
Organisme : European Research Council
ID : 695069
Pays : International
Informations de copyright
© 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.
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