Liraglutide regulates the viability of pancreatic α-cells and pancreatic β-cells through cAMP-PKA signal pathway
| Autor: | Jie Shen, Jinsong Chen, Ming Liang, Xiaozhou Wang, Si Feng, Xiaojun Luan, Lidong Hu, Xuejuan Xu |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cell Survival Apoptosis General Biochemistry Genetics and Molecular Biology Cell Line 03 medical and health sciences Mice Mir-375 Insulin-Secreting Cells Insulin Secretion medicine Cyclic AMP Animals Hypoglycemic Agents Insulin Secretion Viability assay General Pharmacology Toxicology and Pharmaceutics Receptor Cell growth Chemistry Liraglutide Glucagon secretion General Medicine Glucagon Cyclic AMP-Dependent Protein Kinases MicroRNAs 030104 developmental biology Glucagon-Secreting Cells Cancer research medicine.drug Signal Transduction |
| Zdroj: | Life sciences. 195 |
| ISSN: | 1879-0631 |
| Popis: | Aims: As a glucagon-like peptide-1 receptor agonist, liraglutide could effectively increase insulin secretion from pancreatic β-cells and suppress glucagon secretion from pancreatic α-cells in the treatment of hyperglycemia in type 2 diabetes patients. However, the mechanisms for the different regulation of pancreatic α-cells and β-cells are still unclear. In this study, we mainly explored the different effects of liraglutide on mouse pancreatic α-cell line and β-cell line in vitro. Main methods: Herein, mouse pancreatic α-cell line, α-TC1-6, and mouse pancreatic β-cell line, β-TC-tet, were used to analyze the biological effects of liraglutide in different concentrations. Cell proliferation, cell apoptosis and cell secretion ability were detected in different groups. Besides, the level of miR-375 and cAMP-PKA signal pathway were further evaluated using qPCR and western blot. Key findings: The results indicated that liraglutide could increase the level of miR-375 and cell apoptosis in pancreatic α-cells through inhibiting the cAMP-PKA signal pathway, but activate cAMP-PKA signal pathway in pancreatic β-cells, and further lead to the down-regulation of miR-375 and improve cell viability. Therefore, the treatment with liraglutide could down-regulate the glucagon secretion ability of α-TC1-6 cells, and the insulin secretion ability of β-TC-tet cells was enhanced with the liraglutide treatment in a dose-dependent manner. Significance: In conclusion, we mainly found that liraglutide could regulate the viability of pancreatic α-cells and pancreatic β-cells through inhibiting and activating cAMP-PKA signal pathway respectively. The better understanding of the mechanism could help us to develop more novel therapy methods for diabetes in the future. |
| Databáze: | OpenAIRE |
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