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.
Li, Wei; Wang, Jing; Chen, Qiu-Dan; Qian, Xu; Li, Qi; Yin, Yu; Shi, Zhu-Mei; Wang, Lin; Lin, Jie; Liu, Ling-Zhi; and Jiang, Bing-Hua, "Insulin promotes glucose consumption via regulation of miR-99a/mTOR/PKM2 pathway." (2013). Kimmel Cancer Center Faculty Papers. Paper 28.