Research Paper

Genes & Nutrition

, Volume 3, Issue 3, pp 177-180

First online:

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

  • Lukasz WatorAffiliated withDepartment of Clinical Biochemistry, Jagiellonian University Medical College Email author 
  • , Urszula RaznyAffiliated withDepartment of Clinical Biochemistry, Jagiellonian University Medical College
  • , Adriana BalwierzAffiliated withDepartment of Clinical Biochemistry, Jagiellonian University Medical College
  • , Anna PolusAffiliated withDepartment of Clinical Biochemistry, Jagiellonian University Medical College
  • , Hans G. JoostAffiliated withGerman Institute of Human Nutrition
  • , Grzegorz DyduchAffiliated withDepartment of Pathomorphology, Jagiellonian University Medical College
  • , Romana TomaszewskaAffiliated withDepartment of Pathomorphology, Jagiellonian University Medical College
  • , Aldona Dembinska-KiecAffiliated withDepartment of Clinical Biochemistry, Jagiellonian University Medical College

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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