妊娠期糖尿病
胰腺功能
糖尿病
细胞凋亡
下调和上调
后代
医学
PI3K/AKT/mTOR通路
内分泌学
β细胞
妊娠期
胰岛
内科学
怀孕
生物
胰腺
基因
小岛
生物化学
遗传学
作者
Xinmin Cao,Bin Lü,Ying Gu,Xiaodan Li,Dongyan Guo,Fei Xia
出处
期刊:Journal of Environmental Pathology Toxicology and Oncology
[Begell House Inc.]
日期:2022-01-01
卷期号:41 (4): 11-23
被引量:2
标识
DOI:10.1615/jenvironpatholtoxicoloncol.2022041670
摘要
Gestational diabetes mellitus (GDM), a common complication in pregnancy, could threaten the health of both pregnancies and their offspring. miR-210-3p has been reported that play a crucial role in many diseases. Nevertheless, the molecular mechanism and clinical significance of miR-210-3p in the GDM is still unclear. miR-210-3p was overexpressed in the pancreas of the GDM mouse model. Meanwhile, miR-210-3p weakens cell viability and promotes the apoptosis of pancreatic β cells, impairing the function of pancreatic β cells. Bioinformatics analysis showed that miR-210-3p directly targets the expression of Dtx1, and miR-210-3p negatively regulated dtx1. Down-expression of Dtx1 could increase the expression of insulin and boost the function of pancreatic β cells through inhibiting expressions of p-Akt, p-mTOR, p-4E-BP1, and p-SGK1. Rescue experiments verified that miR-210-3p could regulate the function of pancreatic β cells and adjust the content of TG, TC, and HDL in the blood of mice with GDM via regulating the expression of Dtx1. The study demonstrated that miR-210-3p is significantly overexpressed in the pancreas of the GDM mouse model, which could impair the function and cell viability of pancreatic β cells via suppressing the expression of Dtx1 promotes the progression of GDM. These findings provide a novel strategy to treat GDM.
科研通智能强力驱动
Strongly Powered by AbleSci AI