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Liraglutide Improves the Survival of INS-1 Cells by Promoting Macroautophagy.
Int J Endocrinol Metab · 2013
Last updated 2026-08-30In a lab study, the diabetes drug liraglutide helped pancreatic cells survive better by increasing a process called autophagy, which removes damaged parts of cells. When cells were exposed to a fatty acid that normally causes them to die, liraglutide reduced cell death and boosted autophagy. The study used doses of palmitic acid (PA) and liraglutide, but did not specify the exact amounts.
AI summary of the abstract below.
| Journal | Int J Endocrinol Metab, 2013 |
|---|---|
| Citations | 30 |
| Relative citation ratio | 0.84 |
| NIH percentile | 45 |
| Molecules | liraglutide |
Abstract
BACKGROUND: Type 2 diabetes mellitus (T2D) is a metabolic disease characterized by dysfunction of pancreatic beta cell and insulin resistance. Liraglutide, which has many special anti-diabetes biological effects, is found to inhibit beta cell death and ameliorate endoplasmic reticulum stress (ERs) induced by free fatty acid (FFA). Macroautophagy (hereafter referred to as autophagy) altered by FFA is also associated with the dysfunction or death of pancreatic beta cells.
OBJECTIVES: We aim at proving that Liraglutide improves the survival of INS-1 cells by promoting autophagy.
MATERIALS AND METHODS: Cell survival was assessed by CCK8 assay. The percentage of apoptotic cells was determined by flow cytometric assay after Annexin V-FITC/PI staining. Expression of LC3 was detected by western blotting. MDC staining and transmission electron microscopy (TEM) were used in the measurement of autophagy.
RESULTS: Apoptosis induced by PA in INS-1 cells was significantly resolved after Liraglutide treatment. Simultaneously, autophagy was enhanced with the treatment of PA and Liraglutide.
CONCLUSIONS: Liraglutide appears to protect INS-1 cells from apoptosis FFA-induced by promoting autophagy.
CONCLUSIONS: These findings provide a novel role for GLP-1 analogue in preventing or treating with T2D.
Verbatim abstract via PubMed 24348591 ↗
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