Fig. 3

NMN was able to restore reduced NAD concentrations but not cell viability after stimulation with palmitate. NAMPT activity and NAD levels were not involved in hepatic triglyceride storage. a HepG2 cells were either stimulated with palmitate (0.5 mM), the specific NAMPT inhibitor FK866 (10 nM), NMN (0.5 mM) or with the indicated combinations for 48 h. Cell viability and b NAD concentration were measured using WST-1 assay and EnzyChrom™ NAD⁺/NADH Assay Kit (E2ND-100), respectively. c HepG2 cells were stimulated with palmitate (0.5 mM), oleate (1 mM), a combination of both fatty acids (0.5 mM/1 mM), FK866 (10 nM) or with a combination of oleate and FK866. Oil red O staining was performed. Data were normalized to control (serum free medium) which was set 1 and represent three independent experiments performed in triplicates shown as means ± SEM. *p < 0.05, **p < 0.01 compared to control. ^# p < 0.05, ^## p < 0.01 compared to equivalent control (palmitate or FK866)