MicroRNA-191, acting via the IRS-1/Akt signaling pathway, is involved in the hepatic insulin resistance induced by cigarette smoke extract.

Abstract

Cigarette smoke causes insulin resistance, which is associated with type 2 diabetes mellitus (T2DM). However, the mechanism by which this occurs remains poorly understood. Because the involvement of microRNAs (miRNAs) in the development of insulin resistance is largely unknown, we investigated, in hepatocytes, the roles of miR-191 in cigarette smoke extract (CSE)-induced insulin resistance. In L-02 cells, CSE not only decreased glucose uptake and glycogen levels but also reduced levels of insulin receptor substrate-1 (IRS-1) and Akt activation, effects that were blocked by SC79, an activator of Akt. CSE also increased miR-191 levels in L-02 cells. Furthermore, the inhibition of miR-191 blocked the decreases of IRS-1 and p-Akt levels, which antagonized the decreases of glucose uptake and glycogen levels in L-02 cells induced by CSE. These results reveal a mechanism by which miR-191 is involved in CSE-induced hepatic insulin resistance via the IRS-1/Akt signaling pathway, which helps to elucidate the mechanism for cigarette smoke-induced T2DM.

• Authors: Qianlei Yang, Yan Cui, Fei Luo, Xinlu Liu, Qiushi Wang, Jun Bai, Faqin Dong, Qian Sun, Lu Lu, Hui Xu, Junchao Xue, Chao Chen, Quanyong Xiang, Qizhan Liu, Qingbi Zhang
• Journal: Environmental science and pollution research international (Environ Sci Pollut Res Int) Vol. 25 Issue 23 Pg. 22400-22407 (Aug 2018) ISSN: 1614-7499 [Electronic] Germany
• PMID: 28963693 (Publication Type: Journal Article)

Chemical References

• IRS1 protein, human
• Insulin Receptor Substrate Proteins
• MIRN191 microRNA, human
• MicroRNAs
• Glycogen
• Proto-Oncogene Proteins c-akt

Topics

• Cell Line
• Cigarette Smoking (adverse effects)
• Diabetes Mellitus, Type 2 (etiology, metabolism)
• Glycogen (metabolism)
• Hepatocytes (drug effects, metabolism)
• Humans
• Insulin Receptor Substrate Proteins (metabolism)
• Insulin Resistance (genetics)
• MicroRNAs (genetics, metabolism)
• Proto-Oncogene Proteins c-akt (metabolism)
• Signal Transduction (drug effects)