Anti-diabetic actions of glucagon-like peptide-1 on pancreatic beta-cells
Abstract
Glucagon-like peptide-1 (GLP-1), an incretin hormone, is released from intestinal L-cells in response to nutrients. GLP-1 lowers blood glucose levels by stimulating insulin secretion from pancreatic beta-cells in a glucose-dependent manner. In addition, GLP-1 slows gastric emptying, suppresses appetite, reduces plasma glucagon, and stimulates glucose disposal, which are beneficial for glucose homeostasis. Therefore, incretin-based therapies such as GLP-1 receptor agonists and inhibitors of dipeptidyl peptidase IV, an enzyme which inactivates GLP-1, have been developed for treatment of diabetes. This review outlines our knowledge of the actions of GLP-1 on insulin secretion and biosynthesis, beta-cell proliferation and regeneration, and protection against beta-cell damage, as well as the involvement of recently discovered signaling pathways of GLP-1 action, mainly focusing on pancreatic beta-cells.
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DPP-4 inhibitors are employed either as add-on drug therapy when metformin or sulfonylurea is inadequate or as monotherapy in individuals who should not be taking those medications or who are intolerant to them.
“DPP-4 inhibitors are employed either as an add-on drug therapy when metformin (a biguanide), or sulfonylurea is inadequate or as monotherapy in individuals who should not be taking those medications or who are intolerant to them (70).”
GLP-1 stimulates insulin release, inhibits glucagon release, slows gastric emptying, and reduces food intake.
“It stimulates insulin release and secretion in hyperglycemic states, inhibits glucagon release in hyperglycemic or euglycemic states, slows gastric emptying, and reduces food intake.(6, 7)”
From Semaglutide for the treatment of obesity (2023) · cites this paper as [6]
GLP-1 binds to receptors in pancreatic beta cells, gastric mucosa, kidney, heart, and hypothalamus.
“The hormone binds to GLP-1 receptors expressed in tissues such as the pancreatic beta cells, gastric mucosa, kidney, heart, and hypothalamus.(6, 7)”
From Semaglutide for the treatment of obesity (2023) · cites this paper as [6]
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- Authors
- Lee, Y.-S., & Jun, H.-S.
- Affiliations
- Gachon University (KR)
- Corresponding author
- Jun, Hee-Sook
- Venue
- Metabolism
- Publisher
- Elsevier BV
- Published
- 2014-01
- Volume
- 63
- Issue
- 1
- Pages
- 9-19
- ISSN
- 0026-0495 (ISSN-L)
- OpenAlex
- W2063865446
- Cited by
- 315
- References
- 101
- Citations by year
- 2026: 15 · 2025: 34 · 2024: 34 · 2023: 26 · 2022: 28 · 2021: 35 · 2020: 26 · 2019: 21 · 2018: 27 · 2017: 16 · 2016: 17 · 2015: 19 · 2014: 16 · 2013: 1
- FWCI
- 3.11
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- glucagon-like peptide-1, incretins, pancreatic beta cells, insulin secretion, insulin biosynthesis, beta-cell proliferation, beta cell regeneration, beta cell destruction, glucose homeostasis, diabetes treatment, GLP-1 receptor agonists, DPP-4 inhibitors
- MeSH terms
- Insulin Secretion, Animals, Cell Differentiation, Cell Survival, Humans, Hypoglycemic Agents, Insulin, Signal Transduction, Cell Proliferation, Insulin-Secreting Cells, Glucagon-Like Peptide 1, Incretins
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