MicroRNA-34a contributes to the protective effects of glucagon-like peptide-1 against lipotoxicity in INS-1 cells / 中华医学杂志(英文版)
Chinese Medical Journal
;
(24): 4202-4208, 2012.
Article
in English
| WPRIM
| ID: wpr-339870
ABSTRACT
<p><b>BACKGROUND</b>Glucagon-like peptide-1 (GLP-1) reduces fatty acid-induced beta-cell lipotoxicity in diabetes; however, the explicit mechanisms underlying this process are not fully understood. This study was designed to investigate the involvement of microRNA, which regulates gene expression by the sequence-specific inhibition of mRNA transcription in the GLP-1 mediation of beta-cell function.</p><p><b>METHODS</b>The cell viability and apoptosis were determined using an methyl thiazoleterazolium (MTT) assay and flow cytometry. The expression of genes involved in beta-cell function, including microRNA-34a and sirtuin 1, were investigated using real-time PCR. The underlying mechanisms of microRNA-34a were further explored using cell-transfection assays.</p><p><b>RESULTS</b>A 24-hours incubation of INS-1 cells with palmitate significantly decreased cell viability, increased cell apoptosis and led to the activation of microRNA-34a and the suppression of sirtuin 1. A co-incubation with GLP-1 protected the cells against palmitate-induced toxicity in association with a reduction in palmitate-induced activation of microRNA-34a. Furthermore, palmitate-induced apoptosis was significantly increased in cells that were infected with microRNA-34a mimics and decreased in cells that were infected with microRNA-34a inhibitors.</p><p><b>CONCLUSION</b>MicroRNA-34a is involved in the mechanism of GLP-1 on the modulation of beta-cell growth and survival.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Cell Line
/
Cell Survival
/
Apoptosis
/
Palmitic Acid
/
Cell Biology
/
MicroRNAs
/
Insulin-Secreting Cells
/
Glucagon-Like Peptide 1
/
Toxicity
Limits:
Animals
Language:
English
Journal:
Chinese Medical Journal
Year:
2012
Type:
Article
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