The expression of miR-200b-3p is correlated with obesity, but its biological function in the pathogenesis of obesity remains poorly understood. Here we investigated the function of miR-200b-3p in white adipose browning. The C3H10T1/2 and 3T3-L1 cell lines were infected with lentiviruses carrying miR-200b-3p mimic or antisense, then the mRNA and protein expression of adipogenic differentiation genes and brown adipose tissue (BAT)-specific genes were detected. These lentiviruses were also directly injected into the inguinal white adipose tissue (iWAT) of C57BL/6 mice fed a normal chow diet (NCD) or high fat diet (HFD). Body weight, adipose tissue weight, glycolipid metabolism, and related gene expression were measured. Overexpression of miR-200b-3p impaired, whereas inhibition of miR-200b-3p improved white adipose browning both in vitro and in vivo. Mice with overexpression of miR-200b-3p in iWAT showed elevated levels of serum insulin and total cholesterol, and were insulin resistant under HFD. Inhibition of miR-200b-3p in iWAT prevented mice from insulin resistance induced by HFD. Mechanistically, dual-luciferase reporter assay showed that miR-200b-3p directly inhibited Prdm16 expression in the Smad and p38Mapk signaling pathways. In conclusion, our findings suggest that miR-200b-3p regulates adipocyte browning by targeting Prdm16. This could be a potential therapeutic target for obesity.
Qin et al. (Wed,) studied this question.