Fig. 6.

Blocking insulin receptor signaling and oxidative phosphorylation affects the adipogenic potential of BMSCs^adipo progenitors. a Representative pictures and evaluation of Nile Red staining in BMSCs^adipo differentiated in adipogenic conditions (AD) and after 100 nmol·L^–1 S961 (insulin receptor antagonist) treatment (D10), (scale bar 100 μm); b Gene expression of adipocytic and insulin signaling-related genes such as Pparγ2, Fsp27, and Irs1 after S961 treatment; data are presented as the mean of the fold change (F.C.) over undifferentiated cells ± SEM, (n = 3); c representative western blot and densitometry of insulin-stimulated (100 nmol·L^–1, 15 min) phosphorylation of AKT (p-S473AKT) and total AKT and gene expression of Insr in BMSCs^adipo treated with S961 100 nmol·L^–1; (n = 3); d representative pictures and evaluation of Nile Red staining in BMSCs^adipo differentiated in adipogenic conditions (AD) and after 100 ng·mL^–1 oligomycin (inhibitor of ATP-synthase) treatment (D7), (scale bar 100 μm); e gene expression of adipocytic and insulin signaling-related genes such as Pparγ2, Fsp27, and Irs1 after oligomycin treatment; data are presented as the mean fold change (F.C.) over undifferentiated cells ± SEM, (n = 3); f representative western blot and densitometry of insulin-stimulated (100 nmol·L^–1, 15 min) phosphorylation of AKT (p-S473AKT) and total AKT and gene expression of Insr in BMSCs^adipo treated with oligomycin 10 and 100 ng·mL^–1; (n = 2–3); (*P < 0.05, **P < 0.01; ***P < 0.001: CT vs treated cells; two-tailed unpaired Student’s t test)