Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire WELBIO, Université Libre de Bruxelles, Campus Erasme, Route de Lennik 808, B-1070 Brussels, Belgium Université Paris Diderot, Sorbonne Paris-Cité BFA, CNRS EAC 4413, F-75205 Paris, France Euroscreen SA, Brussels, Belgium.
J Endocrinol. 2013 Nov 7;219(3):279-89. doi: 10.1530/JOE-13-0106. Print 2013 Dec.
Chemerin was initially described as a chemoattractant factor for leukocyte populations. More recently, the protein has also been reported to be an adipokine, regulating adipocyte differentiation in vitro via its receptor ChemR23, and to be correlated with BMI and other parameters of the metabolic syndrome in humans. The aim of this study was to investigate the role of the chemerin/ChemR23 axis in the regulation of metabolism in vivo, using a mouse knockout (KO) model for ChemR23 (Cmklr1) in a C57BL/6 genetic background. Body weight and adipose tissue mass did not differ significantly in young animals, but were significantly higher in ChemR23 KO mice aged above 12 months. Glucose tolerance was unaffected. No significant modifications in the levels of blood lipids were observed and no increase in the levels of inflammatory markers was observed in the adipose tissue of KO mice. A high-fat diet did not exacerbate the obese phenotype in ChemR23 KO mice. No obvious defect in adipocyte differentiation was detected, while a marker of lipogenic activity (GPD1 expression) was found to be elevated. In conclusion, the chemerin/ChemR23 system does not appear to play a major role in adipocyte differentiation in vivo, but it may be involved in adipose tissue homeostasis.
趋化素最初被描述为白细胞群体的趋化因子。最近，该蛋白也被报道为一种脂肪因子，通过其受体 ChemR23 调节体外脂肪细胞分化，并与人体的 BMI 和代谢综合征的其他参数相关。本研究的目的是使用 C57BL/6 遗传背景下 ChemR23（Cmklr1）的小鼠敲除（KO）模型，研究趋化素/ChemR23 轴在体内代谢调节中的作用。在年轻动物中，体重和脂肪组织质量没有明显差异，但在 12 个月以上的 ChemR23 KO 小鼠中明显更高。葡萄糖耐量不受影响。在 KO 小鼠的脂肪组织中未观察到血脂水平的显著变化，也未观察到炎症标志物水平的升高。高脂肪饮食并未使 ChemR23 KO 小鼠的肥胖表型恶化。未发现脂肪细胞分化明显缺陷，而脂生成活性的标志物（GPD1 表达）升高。总之，趋化素/ChemR23 系统似乎在体内脂肪细胞分化中不起主要作用，但它可能参与脂肪组织的动态平衡。
