Genes & Nutrition

, Volume 3, Issue 3, pp 177–180

Impaired leptin activity in New Zealand Obese mice: model of angiogenesis

Authors

    • Department of Clinical BiochemistryJagiellonian University Medical College
  • Urszula Razny
    • Department of Clinical BiochemistryJagiellonian University Medical College
  • Adriana Balwierz
    • Department of Clinical BiochemistryJagiellonian University Medical College
  • Anna Polus
    • Department of Clinical BiochemistryJagiellonian University Medical College
  • Hans G. Joost
    • German Institute of Human Nutrition
  • Grzegorz Dyduch
    • Department of PathomorphologyJagiellonian University Medical College
  • Romana Tomaszewska
    • Department of PathomorphologyJagiellonian University Medical College
  • Aldona Dembinska-Kiec
    • Department of Clinical BiochemistryJagiellonian University Medical College
Research Paper

DOI: 10.1007/s12263-008-0103-4

Cite this article as:
Wator, L., Razny, U., Balwierz, A. et al. Genes Nutr (2008) 3: 177. doi:10.1007/s12263-008-0103-4

Abstract

Leptin is prompt to drive angiogenesis, effecting proper vascularisation. Tissue remodeling (including adipose organ) is associated with the angiogenic response. The aim of this study was to investigate the effect of hyperleptinemia on angiogenesis in subcutaneous (s.c.) in vivo matrigel model in mice on a high fat (HF) diet. HF promoted adipose tissue accumulation and biochemical changes resembling metabolic syndrome. However, the impact of this dietary treatment on angiogenesis, measured in s.c. matrigel model was not significant. Changes in leptin concentration were not accompanied by significant angiogenic response. This lack of leptin activity and impaired signal transduction at the molecular level suggests malfunction of the leptin receptor in NZO mice.

Keywords

CD31 PECAM1 Leptin Leptin receptor NZO Obesity

Copyright information

© Springer-Verlag 2008