Extended Data Fig. 2: OXT induces lipolysis through ERK signaling.
From: Control of lipolysis by a population of oxytocinergic sympathetic neurons
a. Glycerol release from cultured mouse adipocytes treated with different doses of OXT for 3 h; n = 3. b. cAMP levels in cultured mouse adipocytes treated with vehicle, 1uM or 10 uM OXT for 15 min; n = 3. c. Western blotting of PKA substrate from cultured adipocytes treated with vehicle or 10uM OXT for 15 min; n = 3. d. Glycerol release from cultured mouse adipocytes treated with vehicle or ISO in the presence of DMSO, PKG inhibitor KT5823 or PKA inhibitor H89; n = 3. Vehicle, ISO vs. control, P < 0.0001; KT5823, ISO vs. Control, P = 0.0001; Vehicle vs. KT5823 after ISO, P = 0.0007; Vehicle vs. H89 after ISO, P < 0.0001. e. Glycerol release from cultured mouse adipocytes treated with vehicle or OXT in the presence of DMSO, PKG inhibitor KT5823 or PKA inhibitor H89; n = 3. Vehicle, OXT vs. control, P = 0.0005; KT5823, OXT vs. control, P = 0.0001; and H89, OXT vs. control, P = 0.0021. f. Dose response for pERK1/2 induced by OXT in cultured mouse adipocytes. Representative image from two western blots. g. Time course of OXT-induced (10 uM) ERK activation and PKA activity in cultured mouse adipocytes. Representative image from two western blots. h. Glycerol release from cultured mouse adipocytes treated with OXT (10 uM), OXT + the MEK inhibitor Trametinib (Tra, 5 nM) or OXT + the ERK inhibitor Temuterkib (Tem, 2 uM); n = 3. Vehicle vs. OXT, P < 0.0001; OXT+Tra vs, OXT alone, P < 0.0001; and OXT+Tem vs. OXT alone, P < 0.0001. Data are presented as mean ± s.e.m. Statistical comparisons were made using 2-tailed Student’s t test. ** denotes P < 0.01; ***P < 0.001, and ****P < 0.0001. For gel source data, see Supplementary Fig. 1.
