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J Endocrinol. 2013 Nov 7;219(3):279-89. doi: 10.1530/JOE-13-0106. Print 2013 Dec.

ChemR23 knockout mice display mild obesity but no deficit in adipocyte differentiation.

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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.


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.


G-protein-coupled receptor; adipokines; inflammation

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