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. 2021 Oct 23;11(11):1573. doi: 10.3390/biom11111573

Figure 5.

Figure 5

Glucocorticoid receptor signaling suppresses adiponectin expression by inactivating PPARγ. (A) The suppressing effects of GCs on adiponectin expression was attenuated by PPARγ agonist rosiglitazone in differentiated 3T3-L1 adipocytes. Cells were treated with 2 μM rosiglitazone for 1 h followed by the co-treatment of 2 μM hydrocortisone for 24 h. (B) The statistical analysis of the results in Figure 5A. White dots, vehicle group (n = 3); gray dots, hydrocortisone group (n = 3); black dots, rosiglitazone group (n = 3); and white square, hydrocortisone and rosiglitazone cotreatment group (n = 3). (C) The inducing effects of mifepristone on adiponectin were suppressed by the treatment of PPARγ antagonist GW9662 in differentiated 3T3-L1 adipocytes. Cells were treated with 20 μM PPARγ antagonist GW9662 for 1 h followed with the co-treatment of 2 μM mifepristone for 24 h. (D) The statistical analysis of the results in Figure 5C. White dots, vehicle group (n = 4); gray dots, mifepristone group (n = 4); black dots, GW9662 group (n = 4); and white square, mifepristone and GW9662 cotreatment group (n = 4). Hydro, hydrocortisone; Ros, rosiglitazone; Mif, Mifepristone; and GW, GW9662. (E) A schematic model showing that cold stress-elevated GCs promote thermogenesis by suppressing adiponectin production. The data in Figure 5B,D are presented as the mean ± S.E.M. * p < 0.05, ** p < 0.01.