Figure 4.

Blockade of WAT CB1R does not modify lipolysis in obese mice and human in vitro. (A) Glycerol production by WAT explants from mice fed with a high fat diet (HFD) and treated 1 hour with vehicle (VEH), Rimonabant (RIMO, 1 µM) or JD5037 (0.3µM) in the presence of norepinephrine (NE, 1 µM). Explants were treated in triplicate and experiments repeated with 3 different HFD mice (n=3/group). ^$p < 0.001 VEH vs other treatments. (B) Glycerol production by abdominal VAT or SAT explants from obese subjects measured in the medium after 1-hour treatment with VEH or RIMO (1 µM) in the presence of NE (1 µM). Explants were treated in triplicate and experiments repeated with tissue from 6 different obese subjects (n=6/group). ^$p < 0.001 VEH vs other treatments. (C) Intracellular cAMP content measured in WAT explants from HFD mice treated 1 hour with VEH, insulin (INS, 1 nM) or RIMO (1 µM) in the presence of NE (1 µM); n=4/group. (D) Intracellular cAMP content measured in WAT explants from HFD mice treated 15 min with VEH, forskolin (FSK, 10 µM) or FSK + RIMO (1 µM); n=5/group. ^$p < 0.001 VEH vs other treatments. (E) Representative immunoblots and densitometry analyses of the phosphorylation level of Akt (T308) in WAT explants collected from HFD mice and treated 20 min with VEH or AEA (5 µM); n=3/group. Results are expressed as mean ± SEM. *p < 0.05.