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Effect of miR-26b on gestational diabetes mellitus in rats via PI3K/Akt signaling pathway
1Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China. evibciq@163.com.
Objective:
The aim of this study was to explore the influence of micro ribonucleic acid (miR)-26b on gestational diabetes mellitus in rats via the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathway.
Materials And Methods:
A total of 60 healthy pregnant female rats were randomly divided into three groups, including group A (normal group), group B (model group), and group C (model + miR-26b group). The differences in fasting blood glucose (FBG), C-reactive protein (CRP), and phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/AKT) among the three groups were analyzed via serum CRP test, morphological observation, quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR), and Western blotting, respectively.
Results:
The levels of FBG ad CRP were significantly up-regulated in group B when compared with group A (p<0.01). Meanwhile, they increased significantly in group C when compared with group B (p<0.01). Rats in group A exhibited smooth and flat thoracic aortic intimas, as well as neatly arranged smooth muscle cells at the media layer. However, rats in group B showed fractured intimas with enlarged junction gaps, as well as necrotic and detached endothelial cells. Compared with group B, group C exhibited extremely poorly arranged cells at all the layers, rough and rugged intimas, larger areas of necrotic and detached endothelial cells, and markedly worsened lesions. QRT-PCR results indicated that the expression of phosphorylated-PI3K (p-PI3K) was significantly lower in group B than that of group A (p=0.04). Meanwhile, it was markedly lower in group C than that in group B (p=0.04). The expression of p-Akt was remarkably lower in group B than group A (p=0.04), which was also significantly lower in group C than group B (p=0.04). Compared with group A, the expressions of p-PI3K and p-Akt in the thoracic aorta of group B were evidently down-regulated (p<0.01). Furthermore, they decreased markedly in group C when compared with group B (p<0.01).
Conclusions:
MiR-26b accelerates the progression of gestational diabetes by inhibiting the PI3K/Akt signaling pathway.
Insights
Micro ribonucleic acid (miR)-26b exacerbates gestational diabetes in rats by inhibiting the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) pathway, worsening vascular damage and metabolic markers.
Area of Science:
- Endocrinology
- Molecular Biology
- Vascular Biology
Background:
- Gestational diabetes mellitus (GDM) poses risks to maternal and fetal health.
- The role of microRNAs (miRNAs) in GDM pathogenesis is an area of active research.
- The phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) pathway is crucial in metabolic regulation.
Purpose of the Study:
- To investigate the effect of miR-26b on GDM in a rat model.
- To elucidate the involvement of the PI3K/Akt signaling pathway in miR-26b's influence on GDM.
Main Methods:
- Utilized a rat model of GDM, with groups including normal, GDM model, and GDM model treated with miR-26b.
- Assessed fasting blood glucose (FBG) and C-reactive protein (CRP) levels.
- Analyzed thoracic aortic intima and media morphology.
- Quantified PI3K/Akt pathway activation using qRT-PCR and Western blotting.
Main Results:
- GDM model rats showed significantly elevated FBG and CRP levels compared to normal rats.
- miR-26b treatment in GDM rats further increased FBG and CRP and worsened vascular lesions.
- Expression of phosphorylated PI3K (p-PI3K) and phosphorylated Akt (p-Akt) was significantly downregulated in GDM rats, with further reduction upon miR-26b administration.
Conclusions:
- MiR-26b accelerates GDM progression in rats.
- The mechanism involves the inhibition of the PI3K/Akt signaling pathway.
- These findings highlight miR-26b as a potential therapeutic target in GDM.
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