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Chinese Medical Journal ; (24): 4202-4208, 2012.
Artículo en Inglés | WPRIM | ID: wpr-339870

RESUMEN

<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>


Asunto(s)
Animales , Ratas , Apoptosis , Línea Celular , Supervivencia Celular , Ácidos Grasos no Esterificados , Toxicidad , Péptido 1 Similar al Glucagón , Farmacología , Células Secretoras de Insulina , Biología Celular , Metabolismo , MicroARNs , Genética , Metabolismo , Ácido Palmítico , Farmacología , Reacción en Cadena en Tiempo Real de la Polimerasa
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