Background 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.Methods 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.Results 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.Conclusion MicroRNA-34a is involved in the mechanism of GLP-1 on the modulation of beta-cell growth and survival.