Genetic and diet effects on Ppar-α and Ppar-γ signaling pathways in the Berlin Fat Mouse Inbred line with genetic predisposition for obesity

Lipids in Health and Disease

Research

Susanne Mauel¹  Achim D Gruber¹  Gudrun A Brockmann²  Armin O Schmitt²  Asja Wagener²  Helge F Goessling²  Richard Reinhardt³ 

[1] Freie Universität Berlin, FB Veterinärmedizin, Institut für Tierpathologie, Robert-von-Ostertag-Straße 15, 14163, Berlin, Germany;Humboldt-Universität zu Berlin, Department for Crop and Animal Sciences, Invalidenstraße 42, 10115, Berlin, Germany;Max-Planck-Institut für molekulare Genetik, Ihnestraße 73, 14195, Berlin, Germany;

关键词: Adipose Tissue;    Fatty Acid Oxidation;    White Adipose Tissue;    Fatty Acid Transport;    Serum Triglyceride Concentration;   

DOI  :  10.1186/1476-511X-9-99

 received in 2010-08-09, accepted in 2010-09-10,  发布年份 2010

来源: Springer

【 摘 要 】

BackgroundThe Berlin Fat Mouse Inbred (BFMI) line is a new mouse model for obesity, which was long-term selected for high fatness. Peroxisome proliferator-activated receptors (PPARs) are involved in the control of energy homeostasis, nutrient metabolism and cell proliferation. Here, we studied the expression patterns of the different Ppar genes and the genes in the PPAR pathway in the BFMI line in comparison to physiological changes.ResultsAt the age of 10 weeks, the BFMI mice exhibited marked obesity with enlarged adipocytes and high serum triglycerides concentrations in comparison to the often used mouse line C57BL/6 (B6). Between these two lines, gene expression analyses revealed differentially expressed genes belonging to the PPAR pathway, in particular genes of the lipogenesis and the fatty acid transport.ConclusionSurprisingly, the Ppar-α gene expression was up-regulated in liver and Ppar-γ gene expression was down-regulated in the white adipose tissue, indicating the activation of a mechanism that counteracts the rise of obesity.

【 授权许可】

Unknown   
© Wagener et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.