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Reduced insulin secretion and content in VEGF-a deficient mouse pancreatic islets

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Jabs,  N
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Lammert,  E
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Citation

Jabs, N., Franklin, I., Brenner, M. B., Gromada, J., Ferrara, N., Wollheim, C. B., et al. (2008). Reduced insulin secretion and content in VEGF-a deficient mouse pancreatic islets. Experimental and Clinical Endocrinology & Diabetes, 116(Suppl. 1), S46-S49.


Cite as: https://hdl.handle.net/21.11116/0000-0001-0E79-9
Abstract
Mice, deficient for vascular endothelial growth factor VEGF-A in pancreatic islets, have reduced insulin gene expression levels and an impaired glucose tolerance. Here, we investigated whether VEGF-A was required for physiological glucose-stimulated insulin secretion and insulin content. We performed in situ pancreas perfusions and islet perifusions on mice lacking VEGF-A in the pancreatic epithelium in order to study their ability to secrete insulin in response to glucose. We identified insulin secretion defects in the pancreata of VEGF-A deficient mice, including a delayed and blunted response to glucose. Islet perifusion experiments revealed a missing first phase and weaker second phase of insulin secretion, in two of three VEGF-A deficient mice. On average, insulin content in VEGF-A deficient islets was significantly reduced when compared with control islets. We conclude that VEGF-A is required in pancreatic islets for normal glucose-stimulated insulin secretion and physiological insulin content. Thus, VEGF-A is a key factor for pancreatic islet function.