Abstract
BackgroundThe 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.MethodsWild-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.ResultsFood intake did not differ between groups. O2 consumption and CO2 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.ConclusionsIn 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.
Highlights
The chemokine receptor CCR7, expressed on various immune cells, is associated with cell migration and lympho-node homing
We previously reported that Ccl19 expression is markedly upregulated in adipocytes co-cultured with macrophages in the presence of toll like receptor-4 ligand, a bacterial endotoxin
The weights of liver and two types of muscle did not differ between the two mouse groups, adipose tissue weights were significantly lower (P values; Epididymal WAT 0.0004, Inguinal WAT 0.0014, and brown adipose tissue (BAT) 0.0216) in KO mice than in WT mice
Summary
The chemokine receptor CCR7, expressed on various immune cells, is associated with cell migration and lympho-node homing. Mice lacking Ccr are protected from diet-induced obesity and subsequent insulin resistance. It is suggested that obesity-induced inflammatory changes accompanied by the infiltration of immune cells into adipose tissue play crucial roles in the establishment of such complications. The number of obese subjects is still increasing in many parts of the world due possibly to the rapid economic changes, and, the development of new and effective therapeutic strategy against obesity and/or insulin resistance is still urgently needed. We believe that adipose tissue browning is one such strategy against obesity. The majority of adipose tissues in adults are believed to be WAT, with abundant triglycerides in adipocytes. The volume of BAT is greater in neonatal infants than in adults, and individual differences in the rate of decline and activity are associated with the development of obesity [1]. The activation of BAT is a therapeutic target for obesity
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