Adipocytes and immune cells are vital for the development of adipose tissue. Adipokines secreted by adipocytes regulate adipogenesis and body metabolism. Chemerin is one of the adipokines. However, the function and mechanism of chemerin in adipose tissue are not fully illuminated. Compared with wild type (WT) mice, Rarres2^−/− mice gained weight and significantly increased fat distribution in subcutaneous adipose tissue (SAT), rather than visceral adipose tissue (VAT) on high fat diet (HFD). PPARγ and C/EBPα, the master regulators of adipogenesis, were up-regulated in SAT and down-regulated in VAT in Rarres2^−/− mice comparing with WT mice. Inspite of chemerin deficiency or not, the ratio of adipocyte-progenitors to total cells and the differentiation capacity of adipocyte-progenitors were similar in SAT and VAT, but macrophage infiltration in VAT was more severe than in SAT in Rarres2^−/− mice. Furthermore, CD45⁺ immune cells supernatant from Rarres2^−/− SAT promoted the differentiation of adipocyte-progenitors and 3T3-L1 cells. Adipokine array assay of CD45⁺ immune cells supernatant revealed that metalloproteinase inhibitor 1 (TIMP1), an inhibitor of adipogenesis, was reduced in Rarres2^−/− SAT, but increased in Rarres2^−/− VAT. As we specifically knocked down chemerin in SAT, TIMP1 was down-regulated and adipogenesis was promoted with reducing infiltration of macrophages. The present study demonstrates that the effects of chemerin on adipose tissue is depot different, and specific knock down chemerin in SAT promote adipogenesis and improve glucose tolerance test (GTT) and insulin tolerance test (ITT). This suggests a potential therapeutic target for chemerin in the treatment of obesity related metabolic disorder.

脂肪细胞和免疫细胞对脂肪组织的发育至关重要。脂肪细胞分泌的脂肪因子调节脂肪生成和身体代谢。Chemerin 是脂肪因子之一。然而，凯莫瑞在脂肪组织中的功能和机制尚未完全阐明。与野生型 (WT) 小鼠相比，Rarres2 ^-/-小鼠体重增加并显着增加皮下脂肪组织 (SAT) 中的脂肪分布，而不是高脂肪饮食 (HFD) 下的内脏脂肪组织 (VAT)。PPARγ 和 C/EBPα 是脂肪生成的主要调节因子，在Rarres2中的 SAT 中上调，而在 VAT 中下调^-/-小鼠与 WT 小鼠进行比较。无论是否缺乏chemerin，脂肪细胞祖细胞与总细胞的比例以及脂肪细胞祖细胞的分化能力在SAT和VAT中相似，但在Rarres2 ^-/-小鼠中，VAT中的巨噬细胞浸润比SAT更严重。此外，来自Rarres2 ^-/- SAT 的CD45 ⁺免疫细胞上清液促进脂肪细胞祖细胞和 3T3-L1 细胞的分化。CD45 ⁺免疫细胞上清液的脂肪因子阵列分析显示，金属蛋白酶抑制剂 1 (TIMP1)，一种脂肪生成抑制剂，在Rarres2 ^-/- SAT 中减少，但在Rarres2 ^{-/- 中}增加增值税。当我们在 SAT 中特异性敲低凯莫瑞时，TIMP1 被下调，脂肪生成随着巨噬细胞浸润的减少而得到促进。本研究表明chemerin对脂肪组织的影响是不同的，SAT中特异性敲低chemerin促进脂肪生成并改善葡萄糖耐量试验（GTT）和胰岛素耐量试验（ITT）。这表明凯莫瑞可作为治疗肥胖相关代谢紊乱的潜在治疗靶点。