Resistin Increases Ectopic Deposition of Lipids Through miR-696 in C2C12 Cells.

Resistin is associated with ectopic deposition of lipids, and determining its developmental and molecular mechanisms may help in the development of novel treatments. MicroRNAs (miRNAs) are involved in many physiological and pathological processes as negative regulators. We performed mouse liver miRNA microarrays to analyze the differences in expression between resistin-treated and control mice; the results showed that miR-696 was significantly upregulated by resistin. Therefore, we aimed to study whether miR-696 played a role in the resistin-induced ectopic deposition of lipids. Quantitative RT-PCR results showed that miR-696 was upregulated both in vivo and in vitro, consistent with the microarray. We transfected C2C12 cells and used miR-696 mimics and inhibitors to assess the role of miR-696 in the resistin-induced ectopic deposition of lipids. The overexpression of miR-696 increased the TG content in C2C12 cells and decreased the mitochondrial content. Next, a study of miR-696's role in the deposition of lipids in C2C12 induced by resistin showed that inhibition of miR-696 restored the TG content by up to 80%, which suggests that, in C2C12 cells, resistin at least partially increases the deposition of lipids through miR-696. miR-696 plays a role in the ectopic deposition of lipids induced by resistin in skeletal muscle at least partially.