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Serum amyloid A3 deficiency impairs in vitro and in vivo adipocyte differentiation
Adipocyte ( IF 3.3 ) Pub Date : 2021-04-25 , DOI: 10.1080/21623945.2021.1916220
Ellen Vercalsteren 1 , Christine Vranckx 1 , Ines Vermeire 2 , Max Gooijen 2 , Roger Lijnen 1 , Ilse Scroyen 1, 2
Affiliation  

ABSTRACT

Obesity, caused by an excess adipose tissue, is one of the biggest health-threats of the 21st century. Adipose tissue expansion occurs through two processes: (i) hypertrophy, and (ii) hyperplasia, the formation of new adipocytes, also termed adipogenesis. Recently, serum amyloid A3 (Saa3) has been implicated in adipogenesis. Therefore, the aim of this study was to investigate the effect of Saa3 on adipogenesis using both an in vitro and in vivo murine model. Saa3 gene silenced pre-adipocytes ha a lower expression of pro-adipogenic markers and less lipid accumulation, indicating impaired adipogenesis. Furthermore, male NUDE mice, injected with Saa3 gene silenced pre-adipocytes developed smaller fat pads with smaller adipocytes and lower expression of pro-adipogenic markers than their control counterparts. This confirms that Saa3 gene silencing indeed impairs adipogenesis, both in vitro and in vivo. These results indicate a clear role for Saa3 in adipogenesis and open new perspectives in the battle against obesity.



中文翻译:

血清淀粉样蛋白 A3 缺乏损害体外和体内脂肪细胞分化

摘要

由过多的脂肪组织引起的肥胖是 21世纪最大的健康威胁之一世纪。脂肪组织扩张通过两个过程发生:(i) 肥大,和 (ii) 增生,即新脂肪细胞的形成,也称为脂肪生成。最近,血清淀粉样蛋白 A3 (Saa3) 与脂肪生成有关。因此,本研究的目的是使用体外和体内鼠模型研究 Saa3 对脂肪生成的影响。Saa3 基因沉默的前脂肪细胞具有较低的促脂肪生成标志物表达和较少的脂质积累,表明脂肪生成受损。此外,与对照组相比,注射了 Saa3 基因沉默前脂肪细胞的雄性 NUDE 小鼠形成了更小的脂肪垫,脂肪细胞更小,促脂肪生成标记物的表达更低。这证实了 Saa3 基因沉默确实损害了体外和体内的脂肪生成。

更新日期:2021-04-26
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