Abstract

Insulin plays an important role in the regulation of glucose metabolism. However, the molecular mechanisms involved are not entirely clarified. In this context, we found that miR-593-3p negatively regulates insulin-regulated glucose metabolism in hepatocellular carcinoma HepG2 and Bel7402 cells. We then identified Slc38a1 and CLIP3 as novel targets of miR-593-3p. Further studies demonstrated that Slc38a1 and CLIP3 mediate insulin-regulated glucose metabolism. Interestingly, we also demonstrated that miR-593-3p expression was negatively associated with Slc38a1 and CLIP3 expression in insulin-treated HepG2 cells, and insulin-induced Slc38a1 and CLIP3 expression via downregulation of miR-593-3p. Taken together, this study indicates that inhibition of miRNA-593-3p by insulin promotes glucose metabolism through the regulation of Slc38a1 and CLIP3 expression, and provides a new insight into the role and mechanism of insulin-induced glycolysis.