The acute glucose lowering effect of specific GPR120 activation in mice is mainly driven by glucagon-like peptide 1
Open accessAbstract
The mechanism behind the glucose lowering effect occurring after specific activation of GPR120 is not completely understood. In this study, a potent and selective GPR120 agonist was developed and its pharmacological properties were compared with the previously described GPR120 agonist Metabolex-36. Effects of both compounds on signaling pathways and GLP-1 secretion were investigated in vitro. The acute glucose lowering effect was studied in lean wild-type and GPR120 null mice following oral or intravenous glucose tolerance tests. In vitro, in GPR120 overexpressing cells, both agonists signaled through Gαq, Gαs and the β-arrestin pathway. However, in mouse islets the signaling pathway was different since the agonists reduced cAMP production. The GPR120 agonists stimulated GLP-1 secretion both in vitro in STC-1 cells and in vivo following oral administration. In vivo GPR120 activation induced significant glucose lowering and increased insulin secretion after intravenous glucose administration in lean mice, while the agonists had no effect in GPR120 null mice. Exendin 9-39, a GLP-1 receptor antagonist, abolished the GPR120 induced effects on glucose and insulin following an intravenous glucose challenge. In conclusion, GLP-1 secretion is an important mechanism behind the acute glucose lowering effect following specific GPR120 activation.
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PUFAs can bind and stimulate G-protein-coupled receptors such as GPR120, leading to increased secretion of glucagon-like peptide 1 from enteroendocrine L-cells.
“Additionally, PUFAs can bind and stimulate G-protein-coupled receptors (GPCRs) which play important roles in regulating glucose metabolism, such as GPR120, thereby leading to increased secretion of the glucagon-like peptide 1 (GLP-1) hormone from enteroendocrine L-cells [50].”
From Mediterranean diet nutrients to turn the tide against insulin resistance and related diseases (2020) · cites this paper as [50]
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References 51 · Cited by 53
- Authors
- Sundström, L., Myhre, S., Sundqvist, M., Ahnmark, A., McCoull, W., Raubo, P., Groombridge, S. D., Polla, M., Nyström, A.-C., Kristensson, L., Någård, M., & Winzell, M. S.
- Affiliations
- AstraZeneca (Sweden) (SE)
- AstraZeneca (United Kingdom) (GB)
- Corresponding author
- Winzell, Maria Sörhede
- Venue
- PLOS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2017-12-05
- Volume
- 12
- Issue
- 12
- Pages
- e0189060
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC5716539
- OpenAlex
- W2773235152
- Cited by
- 53
- References
- 51
- Citations by year
- 2026: 6 · 2025: 4 · 2024: 6 · 2023: 4 · 2022: 8 · 2021: 10 · 2020: 6 · 2019: 7 · 2018: 2
- FWCI
- 3.24
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- AstraZeneca.
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Keywords
- GPR120, glucagon-like peptide-1, GLP-1 secretion, blood glucose reduction, insulin secretion, glucose tolerance, pancreatic islets, Gαq signaling, Gαs signaling, beta-arrestin, cAMP signaling, exendin-9-39
- MeSH terms
- beta-Arrestins, Insulin Secretion, Cyclic AMP, Animals, Blood Glucose, Cell Line, Cricetulus, Female, Glucose Tolerance Test, Humans, Insulin, Islets of Langerhans, Mice, Inbred C57BL, Signal Transduction, CHO Cells, GTP-Binding Proteins, Receptors, G-Protein-Coupled, Mice, Glucagon-Like Peptide 1
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