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Related Experiment Video

Updated: Mar 6, 2026

In situ Quantification of Pancreatic Beta-cell Mass in Mice

In situ Quantification of Pancreatic Beta-cell Mass in Mice

Published on: June 7, 2010

Conditional islet hypovascularisation does not preclude beta cell expansion during pregnancy in mice.

Willem Staels^1,2, Yves Heremans¹, Gunter Leuckx¹

¹Beta Cell Neogenesis (BENE), Vrije Universiteit Brussel, Laarbeeklaan 103, 1090, Brussels, Belgium.

|March 17, 2017

Summary

Reduced vascular endothelial growth factor-A (VEGF-A) signaling causes islet hypovascularization and glucose intolerance in pregnant mice. However, beta cell expansion during pregnancy is not prevented by this condition.

Keywords:

Beta cell FLT1 Islet Pancreas Pregnancy VEGF Vascularisation

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Area of Science:

Endocrinology
Vascular Biology
Reproductive Biology

Background:

Endothelial-endocrine cell interactions and VEGF-A signaling are crucial for maternal islet vascularization, glucose homeostasis, and beta cell expansion during pregnancy.
Understanding the impact of islet vascularization on pregnancy adaptations is vital for managing gestational diabetes.

Purpose of the Study:

To investigate whether pregnancy-associated beta cell expansion is affected by islet hypovascularization.
To determine the role of VEGF-A signaling in regulating maternal islet adaptations during pregnancy.

Main Methods:

Conditional overexpression of soluble fms-like tyrosine kinase 1 (sFLT1), a VEGF-A decoy receptor, in maternal mouse beta cells during pregnancy (embryonic days 1.5-14.5).
Assessment of islet vascularization, glycemic control, beta cell proliferation, individual beta cell size, and total beta cell volume in pregnant and non-pregnant mice.

Main Results:

Overexpression of sFLT1 led to islet hypovascularization and glucose intolerance in both pregnant and non-pregnant mice.
Glucose intolerance in pregnant mice was transient, unlike in non-pregnant littermates.
Beta cell proliferation, individual cell size, and total volume remained unaffected by sFLT1 overexpression during pregnancy.

Conclusions:

Reduced intra-islet VEGF-A signaling causes maternal islet hypovascularization and impairs glycemic control.
Despite hypovascularization, beta cell expansion during mouse pregnancy is not precluded.