Abstract | BACKGROUND AND AIMS: Both cholecystokinin (CCK)-A and CCK-B receptors are expressed in the pancreas, and exogenous gastrin administration stimulates glucagon secretion from human islets. Although gastrin action has been linked to islet neogenesis, transdifferentiation, and beta-cell regeneration, an essential physiologic role(s) for gastrin in the pancreas has not been established. METHODS: RESULTS: CONCLUSIONS: These findings show an essential physiologic role for gastrin in glucose homeostasis; however, the gastrin gene is not essential for murine islet development or the adaptive islet proliferative response to beta-cell injury.
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Authors | Robin P Boushey, Amir Abadir, Daisy Flamez, Laurie L Baggio, Yazhou Li, Veerle Berger, Bess A Marshall, Diane Finegood, Timothy C Wang, Frans Schuit, Daniel J Drucker |
Journal | Gastroenterology
(Gastroenterology)
Vol. 125
Issue 4
Pg. 1164-74
(Oct 2003)
ISSN: 0016-5085 [Print] United States |
PMID | 14517799
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Gastrins
- Insulin
- Receptor, Cholecystokinin B
- Receptors, Cholecystokinin
- Glucagon
- Glucose
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Topics |
- Animals
- Fasting
(physiology)
- Female
- Gastrins
(genetics, metabolism)
- Glucagon
(metabolism)
- Glucose
(metabolism)
- Homeostasis
(physiology)
- Hypoglycemia
(metabolism, physiopathology)
- Insulin
(metabolism)
- Islets of Langerhans
(growth & development, metabolism)
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Mutant Strains
- Receptor, Cholecystokinin B
- Receptors, Cholecystokinin
(metabolism)
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