Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 96, Issue -, Pages 497-502Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2017.10.049
Keywords
Glucagon-like peptide-1; Cholesterol; ATP-binding cassette transporter A1; miR-27a; beta-cell dysfunction
Funding
- National Natural Science Foundation of China (NSFC) [81370902]
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Lipotoxicity is considered one of the main causes of deterioration in beta-cells function. Glucagon-like peptide-1 (GLP-1) has been revealed to protect and improve pancreatic beta-cell function against lipotoxicity. However, the mechanism behind these is largely unknown. The aim of this study was to investigate the effects of GLP-1 on cholesterol-induced lipotoxicity in INS-1 cells and examine the underlying mechanisms. The cell viability was determined, and caspase-3 was used to assess the effects of GLP-1 on cholesterol-induced apoptosis. The alterations of miR-27a and ABCA1 resulting from incubation with cholesterol or GLP-1 were detected by real-time PCR and western blot. The inhibition and overexpression of miR-27a were established to explore the effects of a GLP-1-mediated decrease in miR-27a. Further, Oil red O staining and cholesterol measurement were used to detect lipid accumulation. The beta-cells function was measured in glucose-stimulated insulin secretion. Our data shows that cholesterol significantly attenuated cell viability, promoted cell apoptosis, facilitated lipid accumulation, and impaired beta-cells function, and these effects were significantly reversed by GLP-1. Furthermore, the results demonstrated that GLP-1 decreased miR-27a expression and increased the expression of ABCA1. In conclusion, GLP-1 may affect cholesterol accumulation and beta-cells dysfunction by regulating the expression of miR-27a and ABCA1.
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