期刊
MEDICAL SCIENCE MONITOR
卷 24, 期 -, 页码 2310-2316出版社
INT SCIENTIFIC LITERATURE, INC
DOI: 10.12659/MSM.906286
关键词
Autophagy; Cell Proliferation; Diabetes Mellitus, Type 2; Glucagon-Like Peptide 1; Insulin-Secreting Cells; Cell Proliferation
资金
- United Foundation of the National Natural Science Foundation of China [U1404805]
Background: Clinical and experimental studies have revealed that liraglutide has multiple anti-diabetes biological effects. However, little is known about its role in autophagy and pancreatic beta cell proliferation. This study aimed to assessed the effects of liraglutide on pancreatic b cell proliferation and autophagy in a mouse model of type 2 diabetes. Material/Methods: The effect of liraglutide on autophagy and proliferation in pancreatic beta cells was investigated using a high-fatfed and streptozotocin-induced mouse model of type 2 diabetes. Results: Liraglutide significantly improved the symptoms of high-fat-fed (HFD) and streptozotocin (STZ)-induced type 2 diabetic mice, as indicated by body weight gain, reduction of blood glucose and plasma insulin, and enhanced sensitivity to insulin. The results of quantitative real-time polymerase chain reaction and Western blot analysis showed that liraglutide upregulated AGT5 expression and promoted the conversion of LC3-I to LC3-II, thus improving the defective autophagy. In addition, we observed that both mRNA and protein expressions of PCNA and Ki-67 were upregulated by liraglutide treatment. Immunocytochemical staining results showed that the number of PCNA-or Ki-67-positive cells in pancreatic islet tissues in the HFD + STZ + liraglutide group were increased compared with the HFD + STZ group. Conclusions: These results strongly suggest that liraglutide is able to enhance autophagy and promote pancreatic b cell proliferation. This study improves our insights into the mechanism by which liraglutide treatment relieves diabetes, and provides experimental evidence for clinical utilization of liraglutide in type 2 diabetes treatment.
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