Center for Molecular and Vascular Biology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium.
Health Department, University Colleges Leuven Limburg, Leuven, Belgium.
Adipocyte. 2021 Dec;10(1):242-250. doi: 10.1080/21623945.2021.1916220.
Obesity, caused by an excess adipose tissue, is one of the biggest health-threats of the 21 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.
肥胖是由脂肪组织过度引起的，是 21 世纪最大的健康威胁之一。脂肪组织的扩张通过两种过程发生：（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）已被牵连到脂肪生成中。因此，本研究的目的是使用体外和体内小鼠模型来研究 Saa3 对脂肪生成的影响。Saa3 基因沉默的前脂肪细胞表现出较低的前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，注射了 Saa3 基因沉默的前脂肪细胞的雄性 NUDE 小鼠，其脂肪垫较小，脂肪细胞较小，前脂肪生成标志物的表达也较低，与对照组相比。这证实了 Saa3 基因沉默确实会损害体外和体内的脂肪生成。这些结果表明 Saa3 在脂肪生成中具有明确的作用，并为对抗肥胖开辟了新的视角。
