Fig. 4: Activation of Gq signaling promotes glucose uptake and inhibits lipolysis in 3T3F442A adipocytes.
From: Adipocyte Gq signaling is a regulator of glucose and lipid homeostasis in mice
a 14C-2-Deoxy-D-glucose (2-DG) uptake in GFP- or GqD-expressing 3T3F442A cells after treatment with CNO (10 μM). b–d, 2-DG uptake by CNO (10 μM)-treated GqD-expressing 3T3F442A cells in the presence or absence of the Gq/11 inhibitor FR900359 (FR; 1 μM) (b), BAPTA (Ca2+ chelator, 10 μM) (c), or Compound C (AMPK inhibitor, 10 μM) (d). e CAMKK2 activity of GqD-expressing 3T3F442A cells after treatment with CNO (10 μM) and/or STO-609 (CAMKK2 inhibitor, 2 μM). f Glycerol release after treatment of GqD-expressing 3T3F442A cells with CL316,243 (100 nM) in the presence or absence of CNO (10 μM). g–i Glycerol release after treatment of GqD-expressing 3T3F442A cells with CL316,243 (100 nM), CNO (10 μM), and various pharmacological inhibitors (g: FR, 1 μM; h: STO-609, 2 μM; i: Compound C, 10 μM).). j Plasma FFA levels in adipo-GqD (GqD) and control mice before and after acute CNO injection (10 mg/kg i.p.) (n = 4-8 per group). k Plasma FFA levels in adipo-GqD (GqD) and control mice before and after i.p. treatment with CL316,243 (0.1 μg/kg) plus CNO (10 mg/kg) (n = 8 per group). In (a–i), data were normalized relative to values obtained in the absence of any drugs. Data are presented as means ± s.e.m. of at least three independent experiments (a–i). a, j, k: two-tailed Student’s t-test; b–i: one-way ANOVA followed by Bonferroni’s post-hoc test). Source data are provided as a Source data file.
