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Background  The chemokine receptor CCR7, expressed on various immune cells, is associated with cell migration and lympho-node homing. Mice lacking Ccr7 are protected from diet-induced obesity and subsequent insulin resistance. We evaluated the mechanism underlying these protective effects from the standpoint of energy expenditure.    Methods  Wild-type and Ccr7 null mice were fed a high-fat diet, and the regulation of energy metabolism and energy metabolism-related molecules, e.g., Ucp1,  Cidea , and  Pgc1α , were evaluated.    Results  Food intake did not differ between groups. O 2  consumption and CO 2  production were higher in Ccr7 null mice than in wild-type mice, despite a similar respiratory quotient and glucose and lipid utilization, suggesting that energy expenditure increased in Ccr7 null mice via enhanced metabolism. In white adipose tissues of Ccr7 null mice,  Prdm16 ,  Cd137 ,  Tmem26 ,  Th , and  Tbx1  expression increased. Similarly, in brown adipose tissues of Ccr7 null mice,  Dio2 ,  Pgc1α ,  Cidea ,  Sirt1 , and  Adiponectin  expression increased. In both white and brown adipose tissues, Ucp1 gene and protein expression levels were higher in null mice than in wild-type mice.    Conclusions  In Ccr7 null mice, browning of white adipocytes as well as the activation of brown adipocytes cause enhanced energy metabolism, resulting in protection against diet-induced obesity.    Electronic supplementary material  The online version of this article (10.1186/s12986-019-0372-5) contains supplementary material, which is available to authorized users.

Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure