Figure 3.

Blocking glucocorticoid receptor signaling inhibits cold-induced energy expenditure through upregulating adiponectin. (A) Administration of mifepristone suppressed acute cold-induced O₂ consumption throughout the light and dark cycle. The average O₂ consumption was normalized to whole-body mass. WT + V, wild type mice treated with vehicle; WT + M, wild type mice treated with mifepristone; KO+V, adiponectin KO mice treated with vehicle; KO+M, adiponectin KO mice treated with mifepristone. Under cold conditions, the administration of mifepristone downregulated the expression of thermogenesis genes Ucp1 and Pgc1α, and these effects were diminished in iWAT (B) but not in BAT (C) of adiponectin KO mice. White dots, WT mice with vehicle injection (n = 4); gray dots, WT mice with mifepristone injection (n = 5); black dots, adiponectin KO mice with vehicle injection (n = 4); and white square, adiponectin KO mice with mifepristone injection (n = 4). (D) Treatment of mifepristone increased circulating levels of adiponectin. The data in Figure 3A–C are presented as the mean ± S.E.M. * p < 0.05, ** p < 0.01.