Fig 2: A model depicting the involvement of DA/DAR system in adipocyte functions.DA can reach the adipocytes from infiltrating lymphocyte/macrophages, sympathetic nerve endings or via the circulation in the form of DA-S. DA-S can become de-conjugated to bioactive DA by ARSA which is secreted from the lysosomes. DA binds to either D2R-like or D1R-like membrane receptors. Activation of D2R causes suppression of cAMP and inhibition of PRL gene expression and release. Activation of D1R-like receptors results in the inhibition of leptin release and stimulation of adiponectin and IL-6, an effect which may be mediated via the cGMP or MAPK signaling. Other catecholamines (i.e. NE and Epi) from the circulation or sympathetic neurons activate ß-AR and modulate, by yet an unknown fashion, adipokine release. See text for additional explanations. ARSA, arylsulfatase A; ß-AR, ß-adrenergic receptors; D2R/D1R, type 1 or type 2 dopamine receptors; DA, dopamine; DA-S, dopamine sulfate; Epi, epinephrine; NE, norepinephrine; MAPK, mitogen-activated protein kinase; PRL, prolactin.