Research Paper Volume 13, Issue 1 pp 1357—1368
miR-18a increases insulin sensitivity by inhibiting PTEN
- 1 Department of Radiation and Medical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, China
- 2 Department of Orthopedics, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China
Received: April 19, 2020 Accepted: November 3, 2020 Published: December 3, 2020https://doi.org/10.18632/aging.202319
How to Cite
Copyright: © 2020 Zhou et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The miR-17-92 cluster (miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1 and miR-92a) contributes to the occurrence and development of various diseases by inhibiting multiple target genes. Here, we explored the effects of miR-18a on insulin sensitivity. Quantitative real-time PCR indicated that serum miR-18a levels were lower in type 2 diabetes mellitus patients than in healthy controls, suggesting that miR-18a may influence blood glucose levels. Global overexpression of miR-18a in transgenic mice increased their glucose tolerance and insulin sensitivity, while it reduced expression of the phosphatase and tensin homolog deleted on chromosome ten (PTEN) in their skeletal muscle and adipose tissue. Western blotting indicated that overexpressing miR-18a in 3T3-L1 and C2C12 cells enhanced insulin-stimulated AKT phosphorylation and suppressed PTEN expression, while inhibiting miR-18a had the opposite effects. These results suggest that miR-18a improves insulin sensitivity by downregulating PTEN. This makes miR-18a a potentially useful target for the treatment of diabetes mellitus in the future.