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Insulin promotes glucose consumption via regulation of miR-99a/mTOR/PKM2 pathway.

By Wei Li, Jing Wang, Qiu-Dan Chen, Xu Qian, Qi Li, Yu Yin, Zhu-Mei Shi, Lin Wang, Jie Lin, Ling-Zhi Liu and Bing-Hua Jiang

Abstract

Insulin is known to regulate multiple cellular functions and is used for the treatment of diabetes. MicroRNAs have been demonstrated to be involved in many human diseases, including Type 2 diabetes. In this study, we showed that insulin decreased miR-99a expression levels, but induced glucose consumption and lactate production, and increased the expression of mTOR, HIF-1α and PKM2 in HepG2 and HL7702 cells. Forced expression of miR-99a or rapamycin treatment blocked insulin-induced PKM2 and HIF-1α expression, and glucose consumption and lactate production. Meanwhile, knockdown of HIF-1α inhibited PKM2 expression and insulin-induced glucose consumption. Taken together, these findings will reveal the role and mechanism of insulin in regulating glycolytic activities via miR-99a/mTOR

Topics: Department of Pathology, Anatomy and Cell Biology, Kimmel Cancer Center, Thomas Jefferson University, controlled study; down regulation; gene overexpression; glucose intake; glucose metabolism; glycolysis; human; human cell; insulin response; protein expression; protein function; protein phosphorylation; protein targeting; transcription initiation; upregulation, Other Medical Specialties
Publisher: Jefferson Digital Commons
Year: 2013
OAI identifier: oai:jdc.jefferson.edu:kimmelccfp-1027

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