Extended Data Fig. 5: Effect of OXT on ISO-induced lipolysis.
From: Control of lipolysis by a population of oxytocinergic sympathetic neurons
a. Glycerol release from cultured adipocytes treated with OXT (100 nM), isoproterenol (ISO; 1 uM), or both OXT and ISO; n = 4 biologically independent samples per group. ISO + OXT vs. ISO alone, P < 0.0001. b. Glycerol release from cultured adipocytes treated with varying doses of OXT in the presence or absence of ISO (1uM); n = 3 biologically independent samples per group. P < 0.0001 for all comparisons shown. c. Glycerol release from human adipose explants treated with OXT (10 uM), isoproterenol (ISO; 10 uM), or both in the presence or absence of the MEK inhibitor trametinib (Tra) (5 nM); n = 4. OXT vs. ISO + OXT, P = 0.0002; ISO vs. ISO + OXT, P = 0.0042; ISO + OXT vs. ISO + OXT+Tra, P = 0.0004. d. Glycerol release from human adipose explants treated with different doses of ISO with or without OXT (10 uM); n = 3. ISO 1 uM, P = 0.0054; ISO 10 uM, P < 0.0001. e. Serum FFA levels of female Oxtrflox and OxtrΔAd mice after ISO treatment; n = 5. ISO, P = 0.0044. f. Western blotting of pPLIN1, pHSL, pERK, and PKA activity from the same cells shown in Fig. 1g. Representative image from two western blots. g. Western blotting of pPLIN1, pHSL, pERK, and PKA activity from cultured adipocytes treated with OXT (1 uM), isoproterenol (ISO; 1 uM), or both OXT and ISO, in the presence or absence of the MEK inhibitor Trametinib (Tra; 5 nM) or the ERK inhibitor Temuterkib (Tem; 2 uM). Representative image from two western blots. h. cAMP levels in the same cells shown in Fig. 1g; n = 3 biologically independent samples per group. Data are presented as mean ± s.e.m. Statistical comparisons were made using 2-tailed Student’s t test (a-c,e and h) or 2-way ANOVA (d). ** denotes P < 0.01; ***P < 0.001 and ****P < 0.0001. For gel source data, see Supplementary Fig. 1.
