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Glucagon-like peptide-1 potentiates glucose-stimulated insulin secretion via the transient receptor potential melastatin 2 channel.
- Source :
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Experimental and therapeutic medicine [Exp Ther Med] 2017 Nov; Vol. 14 (5), pp. 5219-5227. Date of Electronic Publication: 2017 Sep 19. - Publication Year :
- 2017
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Abstract
- The transient receptor potential melastatin 2 (TRPM2) channel, a Ca <superscript>2+</superscript> permeable channel activated by cAMP, is expressed on pancreatic β-cells and is responsible for the regulation of insulin secretion. It is known that glucose-stimulated insulin secretion (GSIS) can be potentiated by glucagon like peptide-1 (GLP-1), and that the changes in the extracellular glucose concentration alter the levels of intracellular adenosine ATP and cAMP. The present study hypothesized that TRPM2 mediates the modulatory effect of GLP-1 on insulin secretion. The results demonstrated that silencing of TRPM2 eliminated GLP-1-enhanced insulin secretion, indicating the involvement of TRPM2 in this process. In addition, the results of current recordings of TRPM2 and measurement of the resulting insulin secretion in β-cells in the presence of GLP-1 and various concentrations of glucose suggest that GLP-1 regulates GSIS via the TRPM2 channel. Furthermore, inhibiting the activity or expression of TRPM2 attenuated GLP-1-induced GSIS. By using specific activators or inhibitors, the present study demonstrated that the two primary downstream effectors of the GLP-1 receptor, exchange protein directly activated by cAMP and protein kinase A, differentially influence GSIS and GLP-1-potentiated GSIS. In conclusion, the present study revealed the role of TRPM2 in GLP-1-regulated insulin secretion. The results of the present study provide a novel avenue for the prevention and treatment of diabetes and its complications.
Details
- Language :
- English
- ISSN :
- 1792-0981
- Volume :
- 14
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Experimental and therapeutic medicine
- Publication Type :
- Academic Journal
- Accession number :
- 29201240
- Full Text :
- https://doi.org/10.3892/etm.2017.5136