Open AccessVascular endothelial growth factor B inhibits insulin secretion in MIN6 cells and reduces Ca2+ and cyclic adenosine monophosphate levels through PI3K/AKT pathway
Author(s) -
Jingdan Jia,
Wanglin Jiang,
Xu Luo,
Rongrong Li,
Yuchi Zhao,
Geng Tian,
Yana Li
Publication year - 2021
Publication title -
world journal of diabetes
Language(s) - English
Resource type - Journals
ISSN - 1948-9358
DOI - 10.4239/wjd.v12.i4.480
Subject(s) - medicine , endocrinology , insulin , vascular endothelial growth factor , protein kinase b , secretion , cyclic adenosine monophosphate , pi3k/akt/mtor pathway , signal transduction , biology , microbiology and biotechnology , receptor , vegf receptors
Type 2 diabetes (T2D) is characterized by insufficient insulin secretion caused by defective pancreatic β-cell function or insulin resistance, resulting in an increase in blood glucose. However, the mechanism involved in this lack of insulin secretion is unclear. The level of vascular endothelial growth factor B (VEGF-B) is significantly increased in T2D patients. The inactivation of VEGF-B could restore insulin sensitivity in db/db mice by reducing fatty acid accumulation. It is speculated that VEGF-B is related to pancreatic β-cell dysfunction and is an important factor affecting β-cell secretion of insulin. As an in vitro model of normal pancreatic β-cells, the MIN6 cell line can be used to analyze the mechanism of insulin secretion and related biological effects.