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

ABSTRACT:

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. 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, suggest

SUBMITTER: Sano T 

PROVIDER: S-EPMC6610939 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature