Obesity was originally considered a disease endemic to developed countries but has since emerged as a global health problem. Obesity is characterized by abnormal or excessive lipid accumulation (World Health Organization, WHO) resulting from pre-adipocyte differentiation (adipogenesis). The endoplasmic reticulum (ER) produces proteins and cholesterol and shuttles these compounds to their target sites. Many studies have implicated ER stress, indicative of ER dysfunction, in adipogenesis. Reactive oxygen species (ROS) are also known to be involved in pre-adipocyte differentiation. Prx4 specific to the ER lumen exhibits ROS scavenging activity, and we thereby focused on ER-specific Prx4 in tracking changes in adipocyte differentiation and lipid accumulation. Overexpression of Prx4 reduced ER stress and suppressed lipid accumulation by regulating adipogenic gene expression during adipogenesis. Our results demonstrate that Prx4 inhibits ER stress, lowers ROS levels, and attenuates pre-adipocyte differentiation. These findings suggested enhancing the activity of Prx4 may be helpful in the treatment of obesity; the data also support the development of new therapeutic approaches to obesity and obesity-related metabolic disorders.

中文翻译：

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Peroxiredoxin 4通过调节3T3-L1细胞中的ER应激来抑制胰岛素诱导的脂肪生成。

肥胖最初被认为是发达国家特有的疾病，但此后已成为全球健康问题。肥胖症的特征是脂肪细胞前分化（脂肪生成）导致脂质异常或过量脂质积累（世界卫生组织，世界卫生组织）。内质网（ER）产生蛋白质和胆固醇，然后将这些化合物转运到其靶位。许多研究都暗示在脂肪形成过程中，内质网应激会指示内质网功能障碍。已知活性氧（ROS）也参与了脂肪细胞的分化。特异于ER内腔的Prx4表现出ROS清除活性，因此我们专注于ER特异的Prx4来跟踪脂肪细胞分化和脂质蓄积的变化。Prx4的过表达通过在成脂过程中调节成脂基因的表达来减少内质网应激并抑制脂质蓄积。我们的结果表明，Prx4抑制内质网应激，降低ROS水平，并减弱前脂肪细胞的分化。这些发现表明增强Prx4的活性可能有助于肥胖的治疗。数据还支持开发针对肥胖和与肥胖相关的代谢紊乱的新治疗方法。