遗传和饮食对具有肥胖遗传倾向的柏林肥胖小鼠近交系中 Ppar-α 和 Ppar-γ 信号通路的影响。
Genetic and diet effects on Ppar-α and Ppar-γ signaling pathways in the Berlin Fat Mouse Inbred line with genetic predisposition for obesity.
机构信息
Humboldt-Universität zu Berlin, Department for Crop and Animal Sciences, Invalidenstraße 42, 10115 Berlin, Germany.
出版信息
Lipids Health Dis. 2010 Sep 10;9:99. doi: 10.1186/1476-511X-9-99.
BACKGROUND
The 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.
RESULTS
At 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.
CONCLUSION
Surprisingly, 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.
背景
柏林肥胖小鼠近交系（BFMI）是一种新的肥胖症小鼠模型，该模型经过长期选育以获得高脂肪表型。过氧化物酶体增殖物激活受体（PPARs）参与能量稳态、营养代谢和细胞增殖的调控。在此，我们研究了不同 Ppar 基因的表达模式以及 BFMI 系与生理变化相关的 PPAR 通路中的基因。
结果
在 10 周龄时，与常用的 C57BL/6（B6）小鼠系相比，BFMI 小鼠表现出明显的肥胖，脂肪细胞增大，血清甘油三酯浓度升高。在这两个系之间，基因表达分析显示了属于 PPAR 通路的差异表达基因，特别是脂肪生成和脂肪酸转运的基因。
结论
令人惊讶的是，肝脏中 Ppar-α 基因的表达上调，白色脂肪组织中 Ppar-γ 基因的表达下调，表明存在一种对抗肥胖上升的机制被激活。
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