| Literature DB >> 27613819 |
Xilin Yang1, Zezhang Tao2, Zhanyong Zhu3, Hua Liao1, Yueqiang Zhao4, Huajun Fan4.
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.Entities:
Keywords: CLIP3; Slc38a1; insulin; miR-593-3p
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Year: 2016 PMID: 27613819 DOI: 10.1530/JME-16-0090
Source DB: PubMed Journal: J Mol Endocrinol ISSN: 0952-5041 Impact factor: 5.098