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
Abstract 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‐express...
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| Language: | English |
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Wiley
2020-01-01
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| Series: | Physiological Reports |
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| Online Access: | https://doi.org/10.14814/phy2.14352 |
| _version_ | 1811206881069236224 |
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| author | Ida M. Modvig Charlotte B. Christiansen Jens F. Rehfeld Jens J. Holst Simon Veedfald |
| author_facet | Ida M. Modvig Charlotte B. Christiansen Jens F. Rehfeld Jens J. Holst Simon Veedfald |
| author_sort | Ida M. Modvig |
| collection | DOAJ |
| description | Abstract 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. |
| first_indexed | 2024-04-12T03:54:18Z |
| format | Article |
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| institution | Directory Open Access Journal |
| issn | 2051-817X |
| language | English |
| last_indexed | 2024-04-12T03:54:18Z |
| publishDate | 2020-01-01 |
| publisher | Wiley |
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| series | Physiological Reports |
| spelling | doaj.art-bb223a527af04a8aa09519fd464fd1502022-12-22T03:48:53ZengWileyPhysiological Reports2051-817X2020-01-0182n/an/a10.14814/phy2.14352CCK‐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 colonIda M. Modvig0Charlotte B. Christiansen1Jens F. Rehfeld2Jens J. Holst3Simon Veedfald4Department of Biomedical Sciences The Panum Institute Faculty of Health and Medical Sciences University of Copenhagen Copenhagen DenmarkDepartment of Biomedical Sciences The Panum Institute Faculty of Health and Medical Sciences University of Copenhagen Copenhagen DenmarkDepartment of Clinical Biochemistry Rigshospitalet Copenhagen DenmarkDepartment of Biomedical Sciences The Panum Institute Faculty of Health and Medical Sciences University of Copenhagen Copenhagen DenmarkDepartment of Biomedical Sciences The Panum Institute Faculty of Health and Medical Sciences University of Copenhagen Copenhagen DenmarkAbstract 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.https://doi.org/10.14814/phy2.14352bombesinCCKcholecystokinincolonex vivogastrin |
| spellingShingle | Ida M. Modvig Charlotte B. Christiansen Jens F. Rehfeld Jens J. Holst Simon Veedfald 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 Physiological Reports bombesin CCK cholecystokinin colon ex vivo gastrin |
| title | 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 |
| title_full | 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 |
| title_fullStr | 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 |
| title_full_unstemmed | 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 |
| title_short | 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 |
| title_sort | 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 |
| topic | bombesin CCK cholecystokinin colon ex vivo gastrin |
| url | https://doi.org/10.14814/phy2.14352 |
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