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GLP-1R Agonists Promote Normal and Neoplastic Intestinal Growth through Mechanisms Requiring Fgf7
Open accessAbstract
Glucagon-like peptide-1 (GLP-1) secreted from enteroendocrine L cells promotes nutrient disposal via the incretin effect. However, the majority of L cells are localized to the distal gut, suggesting additional biological roles for GLP-1. Here, we demonstrate that GLP-1 receptor (GLP-1R) signaling controls mucosal expansion of the small bowel (SB) and colon. These actions did not require the epidermal growth factor (EGF) or intestinal epithelial insulin-like growth factor (IGF1) receptors but were absent in Glp1r(-/-) mice. Polyp number and size were increased in SB of exendin-4-treated Apc(Min/+) mice, whereas polyp number was reduced in SB and colon of Glp1r(-/-):Apc(Min/+) mice. Exendin-4 increased fibroblast growth factor 7 (Fgf7) expression in colonic polyps of Apc(Min/+) mice and failed to increase intestinal growth in mice lacking Fgf7. Exogenous exendin-4 and Fgf7 regulated an overlapping set of genes important for intestinal growth. Thus, gain and loss of GLP-1R signaling regulates gut growth and intestinal tumorigenesis.
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“Pancreatic, intestinal, and breast neoplasms were more frequently developed in rodents administered with incretin-based medications”
From Long-Term Efficacy and Safety of Anti-Obesity Treatment: Where Do We Stand? (2021) · cites this paper as [57]
In the citing paper
“these results were not confirmed in human studies [56–58].”
From Long-Term Efficacy and Safety of Anti-Obesity Treatment: Where Do We Stand? (2021) · cites this paper as [57]
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“, 2014) and primates (Pyke et al., 2014), and FGF7 has been detected in the human ENS, raising the possibility that the ENS communicates a GLP-1R-dependent signal that converges on Fgf7 and ultimately promotes crypt fission.”
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Metadata
- Authors
- Koehler, J. A., Baggio, L. L., Yusta, B., Longuet, C., Rowland, K. J., Cao, X., Holland, D., Brubaker, P. L., & Drucker, D. J.
- Affiliations
- Mount Sinai Hospital (CA)
- University of Toronto (CA)
- Corresponding author
- Drucker, Daniel J.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2015-03
- Volume
- 21
- Issue
- 3
- Pages
- 379-391
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W1977144451
- Cited by
- 133
- References
- 53
- Citations by year
- 2026: 10 · 2025: 16 · 2024: 10 · 2023: 9 · 2022: 9 · 2021: 18 · 2020: 11 · 2019: 9 · 2018: 13 · 2017: 6 · 2016: 14 · 2015: 8
- FWCI
- 5.93
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Park Service
- Intarcia Therapeutics
- Merck
- Canadian Institutes of Health Research (12344, MOP 123391)
- Novo Nordisk
- MedImmune
- Ariad Pharmaceuticals
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- GLP-1 receptor, glucagon-like peptide-1, FGF7, exendin-4, intestinal growth, intestinal polyps, intestinal tumorigenesis, ApcMin/+ mice, small intestine, colon, enteroendocrine L cells, incretin effect
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Exenatide, Glucagon-Like Peptide-1 Receptor Agonists, Animals, Colon, Epidermal Growth Factor, Female, Intestinal Mucosa, Intestine, Small, Male, Mice, Inbred C57BL, Peptides, Venoms, Signal Transduction, Receptor, IGF Type 1, Cell Proliferation, Mice, Fibroblast Growth Factor 7, Incretins, Carcinogenesis
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