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Objective  Recent studies have shown that microRNAs (miRNAs/miRs) play key roles in adipogenesis. This study aimed to investigate the role and underlying mechanism of miR‐182 in adipogenesis.    Methods  This study used the 3T3‐L1 cell line and human visceral adipose tissue (VAT)‐derived adipocytes to determine the role of miR‐182 in adipogenesis. Adipose tissues from mice with high‐fat diet–induced obesity, ob/ob mice, or human individuals with obesity were used to determine the association of miR‐182 levels with obesity. A luciferase reporter assay was used to determine the target of miR‐182.    Results  The expression level of miR‐182 was greatly downregulated during white adipogenesis and markedly lower in the VAT of mice and humans with obesity. Ectopic expression of miR‐182 in 3T3‐L1 cells and human adipocytes suppressed the formation of lipid droplets and the expression of adipogenic genes. The luciferase reporter assay showed that miR‐182 targeted the 3′‐untranslated sequence of CCAAT/enhancer‐binding protein α (C/EBPα) directly. In addition, glucocorticoids negatively regulated miR‐182 expression, which, in turn, suppressed the glucocorticoid‐induced expression of C/EBPα.    Conclusions  Taken together, our studies identified miR‐182 as a novel negative regulator of adipogenesis and a potential therapeutic target for obesity.

MicroRNA 182 is a Novel Negative Regulator of Adipogenesis by Targeting CCAAT/Enhancer‐Binding Protein α