Published online Apr 15, 2021. doi: 10.4239/wjd.v12.i4.480
Peer-review started: December 8, 2020
First decision: January 11, 2021
Revised: January 25, 2021
Accepted: March 8, 2021
Article in press: March 8, 2021
Published online: April 15, 2021
Type 2 diabetes (T2D), which is characterized by defective pancreatic β-cell function or insulin resistance leading to insufficient insulin secretion and increased blood sugar, has elicited worldwide public health concerns. Despite the knowledge available on T2D, the mechanism of insulin secretion is still unclear. In this study, we studied the mechanism by which vascular endothelial growth factor B (VEGF-B) affects the insulin secretion signaling pathway in MIN6 cells and explored the role of VEGF-B in blood glucose regulation.
We explored the role of VEGF-B in the insulin secretion signaling pathway and provided mechanistic insights into the occurrence and development of insulin secretion and T2D.
Our aim was to explore the mechanism of insulin secretion, study the effect of VEGF-B on insulin secretion, and provide a new strategy to prevent the progression of T2D.
This study was performed with in vitro cultures of MIN6 cells. By studying the effect of VEGF-B on insulin secretion in MIN6 cells and detecting the levels of Ca2+ and cyclic adenosine monophosphate (cAMP) in the insulin secretion signaling pathway and the expression of key proteins in the PI3K-AKT (phosphatidylinositol 3-kinase-serine/threonine kinase) signaling pathway, the effect of VEGF-B on the insulin secretion mechanism was discussed. Statistical analyses were performed using SPSS statistical software (version 22.0).
In this study, we found that exogenous VEGF-B treatment inhibited the secretion of insulin and simultaneously reduced the levels of Ca2+ and cAMP in MIN6 cells. In MIN6 cells with VEGF-B knockdown, insulin secretion and Ca2+ and cAMP levels increased. The effect of VEGF-B on insulin occurred through the PI3K-AKT pathway.
VEGF-B can inhibit insulin secretion through the PI3K-AKT pathway and may become a new target for the study of T2D. Our study provides new mechanistic insight into insulin secretion.
This study could provide new insights into the mechanism of insulin secretion and form the foundation for new ideas for the prevention of T2D.