ISSN : 2146-3123
E-ISSN : 2146-3131

Inhibiting miR-182-3p Alleviates Gestational Diabetes Mellitus by Improving Insulin Resistance in Skeletal Muscle
Jinghong Rao1, Youfang Chen2, Jingying Huang1, Ruoying Wu1, Zhenzhu Dong1, Yuling Gao1, Xuan Chen1
1Department of Obstetrics and Gynecology Quanzhou First Hospital Affiliated to Fujian Medical University, Fuzhou, China
2Department of Clinical Medicine Quanzhou Medical College, Fuzhou, China
DOI : 10.4274/balkanmedj.galenos.2021.2021-8-140
Pages : 121-129


Background: Gestational diabetes mellitus (GDM) is one of the most common metabolic diseases occurring during pregnancy. MiR-182- 3p participates in a variety of physiological processes such as cell proliferation, apoptosis, differentiation, and migration5, but its role in GDM is largely unknown.
Aims: To investigate the relationship between miRNA-182-3p and GDM and explore a potential therapeutic strategy for GDM.
Study Design: Animal experimentation
Methods: To evaluate the effect of miRNA182-3p in GDM, mice were separated as negative control (NC), miRNA-182-3p mimic or miRNA-182-3p inhibitor, and miRNAs were administered intraperitoneally. Additionally, miRNA-182-3p mimic or miRNA-182-3p inhibitor was transfected into C2C12 cells to evaluate glucose metabolism and insulin-related pathways.
Results: The miR-182-3p mimic accelerated GDM, which was effectively reversed by the inhibitor in GDM mice (P = 0.005, miR- 182-3p inhibitor vs. mimic). Insulin receptor 1 (INSR1) was predicted to be the direct target gene of miR-182-3p using online tools. In addition, the miR-182-3p mimic inhibited INSR1 expression and insulin-related pathways in vivo and in vitro, which were all reversed by the miRNA82-3p inhibitor. Furthermore, the miR-182-3p mimic impaired glucose uptake and consumption by inhibiting translocation of glucose transporter type 4 (GLUT4) toward the C2C12 cell membrane (P = 0.007 vs. control), while the inhibitor accelerated these processes (P = 0.032 vs. control; P = 0.005, miRNA-182-3p inhibitor vs. mimic).
Conclusion: Inhibiting miR-182-3p effectively alleviated the development of GDM through INSR1, suggesting a potential therapeutic strategy for GDM.

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