Thrombosis Research
Volume 127, Supplement 3 , Pages S17-S20, February 2011

Murine models of obesity and hormonal therapy

  • H.R. Lijnen

      Affiliations

    • Corresponding Author InformationCorrespondence: H.R. Lijnen. Center for Molecular and Vascular Biology, KU Leuven, Campus Gasthuisberg, O&N 1, Herestraat 49, Box 911, 3000 Leuven, Belgium. Tel.: +32 16 345771; fax: +32 16 345990

Center for Molecular and Vascular Biology, Katholieke Universiteit Leuven, Leuven, Belgium

Abstract 

Obesity is a common disorder, and related diseases such as diabetes, atherosclerosis, hypertension, cardiovascular disease and cancer are a major cause of mortality and morbidity in Westerntype societies. Development of obesity is associated with extensive modifications in adipose tissue involving adipogenesis, angiogenesis and extracellular matrix proteolysis. The fibrinolytic (plasminogen/plasmin) and matrix metalloproteinase (MMP) systems cooperate in these processes. Adipogenesis is tightly associated with angiogenesis, as shown by the findings that adipose tissue expiants trigger blood vessel formation, whereas in turn adipose tissue endothelial cells promote preadipocyte differentiation. A nutritionally induced obesity model in transgenic mice has been used extensively to study the role of the fibrinolytic and MMP systems and of angiogenesis in the development of obesity. Most studies support a role of these systems in adipogenesis and obesity, and suggest that their modulation may affect development of adipose tissue. Such models have also shown that treatment of obese female mice with estrogens has the potential to improve obesity, insulin resistance and glucose intolerance, via decreased expression of lipogenic genes. Thus, murine models of obesity have been very useful tools to study mechanisms of adipose tissue development, as well as effects of hormonal therapy.

Keywords:  Obesity , Proteases , Angiogenesis , Estrogen

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PII: S0049-3848(11)70006-8

doi:10.1016/S0049-3848(11)70006-8

Thrombosis Research
Volume 127, Supplement 3 , Pages S17-S20, February 2011