Conclusions
Taken together, our studies identified miR-182 as a novel negative regulator of adipogenesis and a potential therapeutic target for obesity.
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.
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.
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.