Insulin Promotes Glucose Consumption via Regulation of miR-99a/mTOR/PKM2 Pathway

被引：32

作者：

Li, Wei ^{[1
]}

Wang, Jing ^{[1
]}

Chen, Qiu-Dan ^{[1
]}

Qian, Xu ^{[1
]}

Li, Qi ^{[1
]}

Yin, Yu ^{[1
]}

Shi, Zhu-Mei ^{[2
]}

Wang, Lin ^{[1
]}

Lin, Jie ^{[4
]}

Liu, Ling-Zhi ^{[3
]}

Jiang, Bing-Hua ^{[1
,3
]}

机构：

[1] Nanjing Med Univ, Dept Pathol, Ctr Canc, Nanjing, Jiangsu, Peoples R China

[2] Nanjing Med Univ, Affiliated Hosp 1, Dept Neurosurg, Nanjing, Jiangsu, Peoples R China

[3] Thomas Jefferson Univ, Kimmel Canc Ctr, Dept Pathol Anat & Cell Biol, Philadelphia, PA 19107 USA

[4] Fujian Normal Univ, Fac Software, Fuzhou, Peoples R China

来源：

PLOS ONE | 2013年 / 8卷 / 06期

基金：

中国国家自然科学基金;

关键词：

PYRUVATE-KINASE M2; HYPOXIA-INDUCIBLE FACTOR-1; FACTOR-I; DIABETES-MELLITUS; MAMMALIAN TARGET; SKELETAL-MUSCLE; METABOLISM; RESISTANCE; MICRORNAS; GROWTH;

D O I：

10.1371/journal.pone.0064924

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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-1 alpha and PKM2 in HepG2 and HL7702 cells. Forced expression of miR-99a or rapamycin treatment blocked insulin-induced PKM2 and HIF-1 alpha expression, and glucose consumption and lactate production. Meanwhile, knockdown of HIF-1 alpha inhibited PKM2 expression and insulin-induced glucose consumption. Taken together, these findings will reveal the role and mechanism ofinsulin in regulating glycolytic activities via miR-99a/mTOR.

引用

页数：8