Ptrf transgenic mice exhibit obesity and fatty liver
Ptrf transgenic mice exhibit obesity and fatty liver
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Ptrf转基因小鼠表现出肥胖和脂肪肝
DOI：
10.1111/1440-1681.12920
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发表时间：
2018-07-01
影响因子：
2.9
通讯作者：
Wang, Miao
中科院分区：
文献类型：
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作者：
Li, Qian;Bai, Lin;Wang, Miao
聚合酶I和转录物释放因子（Ptrf，也称为Cavin1）是小窝生物发生和功能的重要组成部分。PTRF基因敲除小鼠或PTRF突变患者表现出多种病理学，包括显著异常的燃料代谢、脂肪营养不良和肌营养不良。本研究通过构建Ptrf转基因小鼠，探讨其在体内的功能。与野生型（WT）小鼠相比，我们发现Ptrf转基因小鼠表现出肥胖，ALT（丙氨酸氨基转移酶）和AST（天冬氨酸氨基转移酶）水平升高。与WT小鼠相比，PTRF转基因小鼠表现出严重的脂肪变性和肝脏中更高程度的脂肪积累。因此，我们发现脂肪合成基因Fasn在Ptrf转基因小鼠肝脏中的表达增加。因此，Ptrf转基因小鼠将成为研究肥胖和脂肪肝相关疾病的分子机制和治疗靶点的良好模型。
Polymerase I and transcript release factor (Ptrf, also known as Cavin1) is an essential component in the biogenesis and function of caveolae. Ptrf knockout mice or patients with PTRF mutations exhibit numerous pathologies including markedly aberrant fuel metabolism, lipodystrophy and muscular dystrophy. In this study, we generated Ptrf transgenic mice to explore its function in vivo. Compared with wild-type (WT) mice, we found that the Ptrf transgenic mice showed obesity with an increased level of ALT (alanine aminotransferase) and AST (aspartate transaminase). Ptrf transgenic mice exhibited severe fat degeneration and a higher degree of fat accumulation in the liver compared with WT mice. Consistently, we found that the expression of the fat synthesis gene, Fasn, was increased in the liver of Ptrf transgenic mice. Thus, Ptrf transgenic mice would be a good model for investigating the molecular mechanism and therapeutic targets of obesity and fatty liver associated diseases.