Fig. 5: Studies with human adipocytes and primary mouse adipocytes lacking AMPK.
From: Adipocyte Gq signaling is a regulator of glucose and lipid homeostasis in mice
a 2-Deoxy-D-glucose (2-DG) uptake by CNO (10 μM)-treated GqD-expressing, differentiated human white adipocytes (GqD-hWAT cells) in the presence or absence of FR900359 (FR; 1 μM), (BAPTA (10 μM), and Compound C (10 μM). b Glycerol release after treatment of GqD-hWAT cells with isoproterenol (100 nM), CNO (10 μM), and various pharmacological inhibitors (FR, 1 μM; STO-609, 2 μM; Compound C, 10 μM). c Western blot analysis with GqD-expressing primary mouse adipocytes (source: iWAT) demonstrating the lack of all three subunits of AMPK in AMPK KO cells (control = GqD-expressing primary mouse adipocytes with functional AMPK). This experiment was independently repeated twice with similar results. d 2-DG uptake by CNO (10 μM)-treated GqD-expressing primary mouse adipocytes in the presence (control) or absence of AMPK (AMPK KO), either with or without STO-609 (2 μM) co-incubation. e Glycerol release from CNO (10 μM)-treated GqD-expressing primary mouse adipocytes in the presence (control) or absence of AMPK (AMPK KO). Lipolysis was induced by incubation with CL316,243 (100 nM). Experiments were carried out in the absence or presence of STO-609 (2 μM). Glucose uptake and glycerol release data were normalized relative to values obtained in the absence of any drugs. Data are presented as means ± s.e.m. of at least four independent experiments. a, b, d, e: one-way ANOVA followed by Bonferroni’s post-hoc test). Source data are provided as a Source data file.
