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Angiogenesis in the New Zealand obese mouse model fed with high fat diet

Adriana Balwierz1,2 email, Anna Polus1 email, Urszula Razny1 email, Lukasz Wator1 email, Grzegorz Dyduch3 email, Romana Tomaszewska3 email, Stephan Scherneck4 email, Hans Joost4 email and Aldona Dembinska-Kiec1 email

Department of Clinical Biochemistry, Collegium Medicum, Jagiellonian University, Cracow, Poland

Postgraduate School of Molecular Medicine, 61 Żwirki i Wigury Str., 02-091 Warsaw, Poland

Department of Pathomorphology, Collegium Medicum, Jagiellonian University, Cracow, Poland

German Institute of Human Nutrition, Potsdam-Rehbrücke, Germany

author email corresponding author email

Lipids in Health and Disease 2009, 8:13doi:10.1186/1476-511X-8-13

Published: 6 April 2009

Abstract

Background

Obesity and its complications lead to vascular injury, atherosclerosis, diabetes and pathological angiogenesis. One of the models to study the obesity and its entanglements is the New Zealand Obese mice model. Aim of this study was to check the effect of high fat diet on changes in biochemical parameters as well as on process of angiogenesis in NZO mice.

Methods

NZO mice were fed with standard (ST) or high fat (HF) diet for seven weeks. Body weight and serum biochemical parameters were monitored. The PECAM1 positive vessel-like structures immunostaining, as well as the gene expression of the matrigel penetrating cells by microarray (confirmed by real-time PCR method) were analyzed.

Results

Mice fed with HF diet developed obesity. Number of newly created vessels with lumen was correlated with hyperglycemia and animal weight gain. The number of PECAM1 positive cells in matrigel tended to increase during HF diet. Microarray results revealed changes in gene expression (activation of the oxidative stress and insulin resistance, inhibition of apoptosis and cell differentiation), however without markers of endothelial cell network maturation.

Conclusion

Observed changes in the NZO mice on HF diet argue for the hyperglycemia related activation of angiogenesis, leading to the formation of pathological, immature network.


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