Figure 4.

Glucocorticoid receptor signaling transcriptionally suppresses adiponectin in adipocytes. Differentiated 3T3-L1 adipocytes or brown adipocytes were treated with hydrocortisone or mifepristone for 24 h at indicated concentrations. For the co-treatment, 3T3-L1 adipocytes were pre-treated by 2 μM mifepristone for 1 h followed by the co-treatment of 2 μM hydrocortisone. (A) Hydrocortisone treatment suppressed adiponectin mRNA levels in differentiated 3T3-L1 adipocytes in a dose-dependent manner. White dots, vehicle group (n = 3); gray dots, 1 μM hydrocortisone group (n = 3); black dots, 5 μM hydrocortisone group (n = 3); and white square, 10 μM hydrocortisone group (n = 3). Treatment with GC receptor antagonist mifepristone upregulated adiponectin in both mRNA level (B) and protein expression/secretion (C) in a dose-dependent manner in differentiated 3T3-L1 adipocytes. White dots, vehicle group (n = 3); gray dots, 0.1 μM mifepristone group (n = 3); black dots, 1 μM mifepristone group (n = 3); and white square, 2 μM mifepristone group (n = 3). (D) The suppressing effect of hydrocortisone on adiponectin expression and secretion was restored by mifepristone treatment in 3T3-L1 adipocytes. (E) Hydrocortisone treatment suppressed expression and secretion of adiponectin but had no significant effects on the expression of thermogenesis genes in the differentiated brown adipocytes. White dots, vehicle group (n = 3); black dots, hydrocortisone group (n = 3). (F) Mifepristone treatment induced the expression and secretion of adiponectin without significant effects on the expression of thermogenesis genes in the differentiated brown adipocytes. White dots, vehicle group (n = 3); black dots, mifepristone group (n = 3). Veh, vehicle. Hydro, hydrocortisone. Mif, mifepristone. The data in Figure 4A,B,E,F are presented as the mean ± S.E.M. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.