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Insulin promotes glucose consumption via regulation of miR-99a/mTOR/PKM2 pathway.
|Title||Insulin promotes glucose consumption via regulation of miR-99a/mTOR/PKM2 pathway.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Li W, Wang J, Chen Q-D, Qian X, Li Q, Yin Y, Shi Z-M, Wang L, Lin J, Liu L-Z, Jiang B-H|
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.
|Alternate Journal||PLoS ONE|