Published online Nov 15, 2023. doi: 10.4239/wjd.v14.i11.1643
Peer-review started: March 28, 2023
First decision: July 4, 2023
Revised: July 11, 2023
Accepted: September 6, 2023
Article in press: September 6, 2023
Published online: November 15, 2023
Processing time: 230 Days and 17.7 Hours
The results showed that after vascular endothelial growth factor B (VEGFB) overexpression, serum glucose, glucose tolerance, and insulin sensitivity in impaired glucose tolerance (IGT) mice were improved, and the number of secretory granules of β cells was increased by activating the PI3K/AKT signal pathway.
VEGFB can promote insulin-mediated glucagon secretion by activating the PI3K/AKT signaling pathway to improve glucose metabolism in mice with IGT.
This study illustrated the role of VEGFB in regulating insulin-mediated glucagon secretion in mice with IGT by regulating the PI3K/AKT signal pathway, which indicated the regulatory function of VEGFB in improving the IGT condition of mice and preventing the onset of type 2 diabetes in the body. This study proved the molecular mechanism of VEGFB regulating IGT and provided theoretical basis for the treatment of prediabetes.
The research was conducted by Crispr Cas9 and high-fat diet feeding to construct the animal model. Western blot and qRT-PCR were used to detect the expression of proteins and genes. Bioinformatics was used to analyze the correlation between relative proteins in the PI3K/AKT signal pathway.
To specify the underlying mechanism of VEGFB effects on insulin-mediated glucagon secretion in impaired glucose tolerance.
Type 2 diabetes (T2D) can be prevented in pre-diabetic individuals with impaired glucose tolerance. Therefore, converting IGT into a normal condition is critical to prevent the onset of diabetes.
Diabetes is a worldwide health problem, affecting about 415 million people globally. Among them, the number of patients with type 2 diabetes accounts for about 90% of the number of patients with diabetes with a population of 373 million. Pre-diabetes is the main risk factor for progression to type 2 diabetes. Impaired glucose tolerance (IGT) is a pre-diabetes state, and it is mainly manifested as fast blood glucose (FBG) level of<7.0 mmol/L and/or posttraumatic blood glucose (PBG) level of 7.8 – 11.1 mmol/L after 2 h of oral glucose administration. Long-term IGT will greatly increase the risk of type 2 diabetes. Therefore, precision intervention can improve the insulin sensitivity of patients with IGT and effectively prevent or delay the progression to type 2 diabetes. VEGFB, as a novel metabolic regulatory target, has received much attention for its role in regulating insulin sensitivity. Therefore, we successfully constructed a mouse model with IGT, and intervened in the upregulation and downregulation of the VEGFB gene at the gene level, so as to explore that VEGFB regulates insulin-mediated Glucagon secretion, and thus improves IGT symptoms in pre-diabetes.