Jia JD, Jiang WG, Luo X, Li RR, Zhao YC, Tian G, Li YN. Vascular endothelial growth factor B inhibits insulin secretion in MIN6 cells and reduces Ca2+ and cyclic adenosine monophosphate levels through PI3K/AKT pathway. World J Diabetes 2021; 12(4): 480-498 [PMID: 33889292 DOI: 10.4239/wjd.v12.i4.480]
Corresponding Author of This Article
Ya-Na Li, PhD, Associate Professor, Department of Pathophysiology, School of Basic Medicine, Binzhou Medical University, No. 346 Guanhai Road, Laishan District, Yantai 264003, Shandong Province, China. yaya-698@163.com
Research Domain of This Article
Pathology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Apr 15, 2021; 12(4): 480-498 Published online Apr 15, 2021. doi: 10.4239/wjd.v12.i4.480
Vascular endothelial growth factor B inhibits insulin secretion in MIN6 cells and reduces Ca2+ and cyclic adenosine monophosphate levels through PI3K/AKT pathway
Jing-Dan Jia, Xu Luo, Rong-Rong Li, Ya-Na Li, Department of Pathophysiology, School of Basic Medicine, Binzhou Medical University, Yantai 264003, Shandong Province, China
Wen-Guo Jiang, Geng Tian, Department of Pharmacy, Binzhou Medical University, Yantai 264003, Shandong Province, China
Yu-Chi Zhao, Department of Surgery, Yantaishan Hospital, Yantai 264001, Shandong Province, China
Author contributions: Li YN and Tian G conceived and designed the study; Jia JD, Luo X, and Li RR performed the experiments; Jiang WG and Zhao YC analyzed the data; Jia JD wrote the manuscript; Li YN revised the manuscript; all authors approved the final version of the article.
Supported byNational Natural Science Foundation of China, No. 31771284; National Natural Science Foundation of China Youth Project, No. 31702024; Major Basic Research Project of Shandong Provincial Natural Science Foundation, No. ZR2019ZD27; and Shandong Province Higher Educational Science and Technology Plan Project, No. J17KA258.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board of Binzhou Medical University.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Medical Ethics Committee of Binzhou Medical University (IACUC protocol number: 2017-018).
Conflict-of-interest statement: The authors declare that they have no conflicts of interest to disclose.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Corresponding author: Ya-Na Li, PhD, Associate Professor, Department of Pathophysiology, School of Basic Medicine, Binzhou Medical University, No. 346 Guanhai Road, Laishan District, Yantai 264003, Shandong Province, China. yaya-698@163.com
Received: December 8, 2020 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 Processing time: 121 Days and 18.1 Hours
ARTICLE HIGHLIGHTS
Research background
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.
Research motivation
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.
Research objectives
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.
Research methods
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).
Research results
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.
Research conclusions
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.
Research perspectives
This study could provide new insights into the mechanism of insulin secretion and form the foundation for new ideas for the prevention of T2D.
