These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: MicroRNA-125b-5p improves pancreatic β-cell function through inhibiting JNK signaling pathway by targeting DACT1 in mice with type 2 diabetes mellitus.
    Author: Yu CY, Yang CY, Rui ZL.
    Journal: Life Sci; 2019 May 01; 224():67-75. PubMed ID: 30684546.
    Abstract:
    Type 2 diabetes mellitus (T2DM) is a progressive disease, accompanied by increased insulin resistance and deteriorating β-cell function. Previous studies have revealed that microRNA (miRNA) plays a crucial role in the treatment of T2DM. Hence, we aim to investigate the role of microRNA-125b-5p (miR-125b-5p) in pancreatic β-cell function and insulin sensitivity of mice with T2DM with the involvement of Dishevelled antagonist Dapper1 (DACT1) and the c-Jun NH2-terminal kinases (JNK) signaling pathway. Firstly, a mouse model of T2DM was established by administering a high-fat diet plus low dosage of streptozotocin, and function of pancreatic β-cell and insulin sensitivity in the normal and T2DM mice were detected. Then, the pancreatic β-cells were collected from pancreatic islet tissues and treated with different mimics, inhibitors and siRNAs. After that, the relationship among miR-125b-5p, DACT1, and the JNK signaling-related factors in T2DM mice was determined. Finally, cell proliferation and apoptosis were determined. Mice with T2DM had lower pancreatic β-cell function and insulin sensitivity, as well as diminished expression of miR-125b-5p but enhanced expressions of DACT1, JNK and c-Jun. miR-125b-5p inhibited DACT1 expression and the activation of the JNK signaling pathway, as well as restrained cell proliferation and promoted cell apoptosis. The current results suggest that up-regulated miR-125b-5p promotes insulin sensitivity and enhances pancreatic β-cell function through inhibiting the JNK signaling pathway by negatively mediating DACT1.
    [Abstract] [Full Text] [Related] [New Search]