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Identification and Characterization of GLP-1 Receptor–Expressing Cells Using a New Transgenic Mouse Model
Open accessAbstract
GLP-1 is an intestinal hormone with widespread actions on metabolism. Therapies based on GLP-1 are highly effective because they increase glucose-dependent insulin secretion in people with type 2 diabetes, but many reports suggest that GLP-1 has additional beneficial or, in some cases, potentially dangerous actions on other tissues, including the heart, vasculature, exocrine pancreas, liver, and central nervous system. Identifying which tissues express the GLP-1 receptor (GLP1R) is critical for the development of GLP-1–based therapies. Our objective was to use a method independent of GLP1R antibodies to identify and characterize the targets of GLP-1 in mice. Using newly generated glp1r-Cre mice crossed with fluorescent reporter strains, we show that major sites of glp1r expression include pancreatic β- and δ-cells, vascular smooth muscle, cardiac atrium, gastric antrum/pylorus, enteric neurones, and vagal and dorsal root ganglia. In the central nervous system, glp1r-fluorescent cells were abundant in the area postrema, arcuate nucleus, paraventricular nucleus, and ventromedial hypothalamus. Sporadic glp1r-fluorescent cells were found in pancreatic ducts. No glp1r-fluorescence was observed in ventricular cardiomyocytes. Enteric and vagal neurons positive for glp1r were activated by GLP-1 and may contribute to intestinal and central responses to locally released GLP-1, such as regulation of intestinal secretomotor activity and appetite.
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“GLP-1 also decreases hepatic glucose production by inhibiting glucagon secretion from α cells, and increases insulin sensitivity in skeletal muscle through an indirect mechanism by increasing microvascular recruitment in skeletal muscle which may potentiate local insulin action.7”
From GLP-1 single, dual, and triple receptor agonists for treating type 2 diabetes and obesity: a narrative review (2024) · cites this paper as [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“GLP-1 also decreases hepatic glucose production by inhibiting glucagon secretion from α cells, and increases insulin sensitivity in skeletal muscle through an indirect mechanism by increasing microvascular recruitment in skeletal muscle which may potentiate local insulin action.7”
From GLP-1 single, dual, and triple receptor agonists for treating type 2 diabetes and obesity: a narrative review (2024) · cites this paper as [7]
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“The receptors to these peptides are expressed locally in the gut enteric neurons and vagal afferents, as well as in the central nervous system (CNS), including the brainstem and hypothalamus (De Silva and Bloom, 2012;Richards et al., 2014).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Richards et al., 2014
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“GLP-1 directly acts on pancreatic β-cells to enhance insulin secretion.”
From GLP-1 single, dual, and triple receptor agonists for treating type 2 diabetes and obesity: a narrative review (2024) · cites this paper as [7]
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“These cells produce serotonin, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), affecting brain function and behavior [89,90,136].”
From Unraveling the Connections: Eating Issues, Microbiome, and Gastrointestinal Symptoms in Autism Spectrum Disorder (2025) · cites this paper as [90]
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Metadata
- Authors
- Richards, P., Parker, H. E., Adriaenssens, A. E., Hodgson, J. M., Cork, S. C., Trapp, S., Gribble, F. M., & Reimann, F.
- Affiliations
- Addenbrooke's Hospital (GB)
- University College London (GB)
- Corresponding author
- Gribble, Fiona M.
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2014-03-13
- Volume
- 63
- Issue
- 4
- Pages
- 1224-1233
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC4092212
- OpenAlex
- W2146534889
- Cited by
- 472
- References
- 28
- Citations by year
- 2026: 29 · 2025: 37 · 2024: 41 · 2023: 20 · 2022: 46 · 2021: 49 · 2020: 44 · 2019: 32 · 2018: 47 · 2017: 34 · 2016: 32 · 2015: 33 · 2014: 27
- FWCI
- 24.43
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Diabetes (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Apollo (University of Cambridge) (submittedVersion)
- Funders
- Wellcome Trust (WT088357Z/09/Z, 088357, WT084210Z/07/Z, 084210)
- Medical Research Council (MR/J013293/2, MR/J013293/1)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- GLP-1 receptor, pancreatic beta cells, pancreatic delta cells, enteric neurons, vagal ganglia, dorsal root ganglia, vascular smooth muscle, area postrema, arcuate nucleus, paraventricular nucleus, ventromedial hypothalamus, GLP-1 signaling, appetite regulation, type 2 diabetes
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Animals, Central Nervous System, Heart Atria, Islets of Langerhans, Mice, Transgenic, Muscle, Smooth, Vascular, Receptors, Glucagon, Mice
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