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Cited by 126Pancreatic function and diabetesDiabetes Treatment and ManagementDiabetes and associated disorders

The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.

Glucose-dependent insulinotropic polypeptide receptor null mice exhibit compensatory changes in the enteroinsular axis

Pamir, Nathalie, Lynn, Francis C., Buchan, Alison M. J., Ehses, Jan, Hinke, Simon A., Pospisilik, J. Andrew, Miyawaki, Kazumasa, Yamada, Yuichiro, Seino, Yutaka, McIntosh, Christopher H. S., Pederson, Raymond A.·2003·American Journal of Physiology-Endocrinology and Metabolism
DOI 10.1152/ajpendo.00270.2002
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Abstract

The incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are gut hormones that act via the enteroinsular axis to potentiate insulin secretion from the pancreas in a glucose-dependent manner. Both GLP-1 receptor and GIP receptor knockout mice ( GLP-1R −/− and GIPR −/− , respectively) have been generated to investigate the physiological importance of this axis. Although reduced GIP action is a component of type 2 diabetes, GIPR-deficient mice exhibit only moderately impaired glucose tolerance. The present study was directed at investigating possible compensatory mechanisms that take place within the enteroinsular axis in the absence of GIP action. Although serum total GLP-1 levels in GIPR knockout mice were unaltered, insulin responses to GLP-1 from pancreas perfusions and static islet incubations were significantly greater (40–60%) in GIPR −/− than in wild-type ( GIPR +/+ ) mice. Furthermore, GLP-1-induced cAMP production was also elevated twofold in the islets of the knockout animals. Pancreatic insulin content and gene expression were reduced in GIPR −/− mice compared with GIPR +/+ mice. Paradoxically, immunocytochemical studies showed a significant increase in β-cell area in the GIPR-null mice but with less intense staining for insulin. In conclusion, GIPR −/− mice exhibit altered islet structure and topography and increased islet sensitivity to GLP-1 despite a decrease in pancreatic insulin content and gene expression.

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Crossref · 10.1152/ajpendo.00270.2002

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Research works printed but not linked: 3

  1. 10.1111/j.1572-0241.1999.01043.x · DOI
  2. Trumper A, 2001, Mol Endocrinol, 15, 1559
  3. Willms B, 1996, J Clin Endocrinol Metab, 81, 327

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Metadata

Authors
Pamir, N., Lynn, F. C., Buchan, A. M. J., Ehses, J., Hinke, S. A., Pospisilik, J. A., Miyawaki, K., Yamada, Y., Seino, Y., McIntosh, C. H. S., & Pederson, R. A.
Affiliations
  • University of British Columbia (CA)
  • Kyoto University (JP)
ORCID
Venue
American Journal of Physiology-Endocrinology and Metabolism
Publisher
American Physiological Society
Published
2003-05-01
Volume
284
Issue
5
Pages
E931-E939
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
DOI
10.1152/ajpendo.00270.2002
OpenAlex
W2098266516
Cited by
126
References
47
Citations by year
2026: 4 · 2025: 6 · 2024: 5 · 2023: 4 · 2022: 6 · 2021: 6 · 2020: 3 · 2019: 7 · 2018: 7 · 2017: 4 · 2016: 7 · 2015: 7 · 2014: 2 · 2013: 2 · 2012: 4
FWCI
5.75
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords
glucose-dependent insulinotropic polypeptide, enteroinsular axis, glucagon-like peptide-1, GLP-1 receptor, pancreatic beta cells, insulin secretion, compensatory mechanisms, cAMP signaling, type 2 diabetes, incretins
MeSH terms
Adaptation, Physiological, Cyclic AMP, Animals, Arginine, Gastric Inhibitory Polypeptide, Glucagon, Glucose, Glucose Tolerance Test, Immunohistochemistry, Insulin, Intestines, Intracellular Membranes, Islets of Langerhans, Mice, Inbred C57BL, Pancreas, Peptide Fragments, Protein Precursors, Receptors, Gastrointestinal Hormone, RNA, Messenger, Mice, Knockout, Mice, Glucagon-Like Peptide 1, In Vitro Techniques

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