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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.

world journal of diabetes

Vascular endothelial growth factor B inhibits insulin secretion in MIN6 cells and reduces Ca<sup>2+</sup> and cyclic adenosine monophosphate levels through PI3K/AKT pathway

Vascular endothelial growth factor B inhibits insulin secretion in MIN6 cells and reduces Ca2+ and cyclic adenosine monophosphate levels through PI3K/AKT pathway

Vascular endothelial growth factor B inhibits insulin secretion in MIN6 cells and reduces Ca²⁺ and cyclic adenosine monophosphate levels through PI3K/AKT pathway