Related Experiment Video
Updated: May 14, 2026
Co-staining Blood Vessels and Nerve Fibers in Adipose Tissue
Published on: February 13, 2019
Effect of vascular endothelial growth factor receptor 2 antagonism on adiposity in obese mice
1Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, KU Leuven, Campus Gasthuisberg, Onderwijs & Navorsing 1, Herestraat 49, Box 911, B-3000 Leuven, Belgium. roger.lijnen@med.kuleuven.be
Abstract:
Development and maintenance of fat depots require angiogenesis, in which vascular endothelial growth factor (VEGF) and its receptors play a crucial role. We have evaluated the effect of blocking VEGF receptor 2 (VEGF-R2) with a MAB (DC101) on adipose tissue of mice with established obesity. Therefore, obese male wild-type C57B1/6 mice were treated with i.p. injection of DC101 (40 mg/kg body weight, twice weekly during 13 weeks) or of the control antibody 1C8. Treatment with DC101 resulted in a slightly lower body weight but had no effect on subcutaneous (SC) or gonadal (GON) white adipose tissue mass, as monitored by MRI. Histochemical analysis of isolated SC and GON fat pads did not reveal significant effects of DC101 treatment on adipocyte or blood vessel size or density. Plasma levels of the liver enzymes aspartate aminotransferase and alanine aminotransferase as well as liver triglyceride levels were significantly decreased following DC101 treatment. Plasma glucose levels were markedly lower upon DC101 treatment, whereas insulin and adiponectin levels were not affected. Furthermore, Akt phosphorylation in adipose tissues was not affected. Thus, in vivo VEGF-R2 blockade in mice with established nutritionally induced obesity did not significantly affect insulin signaling in adipose tissue or adiposity.
Insights
Blocking vascular endothelial growth factor receptor 2 (VEGF-R2) in obese mice did not alter adipose tissue mass or insulin signaling. However, it did reduce liver enzymes and improve glucose levels, suggesting metabolic benefits beyond fat regulation.
Area of Science:
- Metabolic research
- Angiogenesis research
- Obesity research
Background:
- Fat depot development relies on angiogenesis, with vascular endothelial growth factor (VEGF) and its receptors being key players.
- VEGF receptor 2 (VEGF-R2) is implicated in the vascularization of adipose tissue.
Purpose of the Study:
- To investigate the impact of blocking VEGF-R2 on established obesity in mice.
- To assess the effects of VEGF-R2 blockade on adipose tissue mass, cellularity, and insulin signaling.
Main Methods:
- Obese male C57B1/6 mice were treated with a VEGF-R2 blocking monoclonal antibody (DC101) or a control antibody for 13 weeks.
- Body weight, adipose tissue mass (subcutaneous and gonadal), adipocyte size, and blood vessel density were assessed.
- Plasma levels of liver enzymes, triglycerides, glucose, insulin, and adiponectin were measured. Akt phosphorylation in adipose tissue was also analyzed.
Main Results:
- DC101 treatment led to a slight decrease in body weight but did not significantly affect white adipose tissue mass, adipocyte size, or blood vessel density.
- Significant reductions in plasma liver enzymes (AST, ALT) and liver triglycerides were observed.
- Plasma glucose levels were markedly lower in the DC101 group, while insulin and adiponectin levels remained unchanged.
- Akt phosphorylation in adipose tissue was not affected by DC101 treatment.
Conclusions:
- In vivo blockade of VEGF-R2 in established obesity does not significantly impact adipose tissue mass or insulin signaling.
- VEGF-R2 inhibition may offer metabolic benefits, including improved glucose homeostasis and reduced liver steatosis, independent of changes in adiposity.
