State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen 361102, China.
Laboratory Animal Center, Xiamen University, Xiamen 361102, China.
Int J Mol Sci. 2022 Jun 12;23(12):6563. doi: 10.3390/ijms23126563.
Decidual protein induced by progesterone (DEPP) was originally identified as a modulator in the process of decidualization in the endometrium. Here, we define that DEPP is involved in adipose tissue thermogenesis, which contributes to metabolic regulation. Knockdown of DEPP suppressed adipocyte differentiation and lipid accumulation in 3T3-L1 cells, induced expression of brown adipose tissue (BAT) markers in primary brown adipocyte and induced mouse embryonic fibroblasts (MEFs) differentiation to brown adipocytes. Moreover, DEPP deficiency in mice induced white adipocyte browning and enhanced BAT activity. Cold exposure stimulated more browning of white adipose tissue (WAT) and maintained higher body temperature in DEPP knockout mice compared to that in wild-type control mice. DEPP deficiency also protected mice against high-fat-diet-induced insulin resistance. Mechanistic studies demonstrated that DEPP competitively binds SIRT1, inhibiting the interaction between peroxisome proliferator-activated receptor gamma (PPARγ) and Sirtuin 1 (SIRT1). Collectively, these findings suggest that DEPP plays a crucial role in orchestrating thermogenesis through regulating adipocyte programs and thus might be a potential target for the treatment of metabolic disorders.
孕激素诱导的蜕膜蛋白(DEPP)最初被鉴定为子宫内膜蜕膜化过程中的调节剂。在这里,我们定义 DEPP 参与脂肪组织产热,有助于代谢调节。DEPP 的敲低抑制了 3T3-L1 细胞中的脂肪细胞分化和脂质积累,诱导原代棕色脂肪细胞中棕色脂肪组织(BAT)标志物的表达,并诱导小鼠胚胎成纤维细胞(MEFs)分化为棕色脂肪细胞。此外,小鼠中 DEPP 的缺失诱导白色脂肪细胞褐变并增强 BAT 活性。与野生型对照小鼠相比,冷暴露刺激白色脂肪组织(WAT)更多褐变,并维持 DEPP 敲除小鼠更高的体温。DEPP 缺失还可防止高脂肪饮食诱导的胰岛素抵抗。机制研究表明,DEPP 通过竞争性结合 SIRT1 来抑制过氧化物酶体增殖物激活受体 γ(PPARγ)与 Sirtuin 1(SIRT1)之间的相互作用。总之,这些发现表明 DEPP 通过调节脂肪细胞程序在协调产热中起关键作用,因此可能是治疗代谢紊乱的潜在靶标。