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ession between resistin-treated and control mice, and results showed miR-34a to be upregulated by resistin. The purpose of this study was to determine whether miR-34a played a role in resistin-induced decrease of ATP contents. Transient transfection of miR-34a mimics was used to overexpress miR-34a and quantitative RT-PCR was used to detect its expression. Western blot analysis was used to determine the rate of expression at the protein level. ATP content was measured using an ATP assay kit. The target gene of miR-34a was analyzed using bioinformatics and confirmed with dual-luciferase report system. MiR-34a was upregulated by resistin in HepG2 cells, and overexpression of miR-34a was found to diminish ATP levels significantly. This study is the first to show that ATP5S is one of the target genes of miR-34a. Resistin diminishes ATP content through the targeting of ATP5S mRNA 3'UTR by miR-34a.