Abstract

Leptin is secreted by adipose tissue, regulates food intake, and increases secretion of pro‐inflammatory cytokines. Mouse adipocytes expressed dopamine D2 receptors (D2R). Therefore, we aimed to determine the role of the D2Rs on the regulation of the expression of leptin, adiponectin, and other pro‐inflammatory cytokines in adipocytes. For this experiments mouse 3T3‐L1 cells were cultured to 100% confluency, differentiated to adipocytes for 3 days, and studied 8 days after differentiation. Stimulation of D2Rs with quinpirole (1ìM, 24h) increased the expression of leptin both in cells (23±8%, P<0.05; western blot) and in the media (59±4pg/ml vs. 45±3pg/ml, P<0.05, ELISA), as well as the expression of IL‐6 (49±7%, P<0.05, western blot), but did not modify that of adiponectin. The effects were prevented by the D2R selective antagonist (L741,626). D2R stimulation also increased gene expression (qRT‐PCR) of leptin (1.50±0.03 fold, P<0.05), IL‐6 (2.44±0.08 fold, P<0.05), TNF alpha (2.23±0.06 fold, P<0.05), MCP1 (1.82±0.04 fold, P<0.05), MCP2 (2.43±0.06 fold, P<0.05) and NFkB p50 (1.47±0.02 fold, P<0.05). Adipocyte D2R positively regulates the expression of leptin and pro‐inflammatory cytokines and chemokines in 3T3‐L1. In contrast renal D2R inhibits the their expression. We suggest that the effect of D2R is tissue‐specific but the mechanism involved is undetermined.

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