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. Author manuscript; available in PMC: 2017 May 26.
Published in final edited form as: Biochim Biophys Acta. 2015 Sep 6;1853(11 Pt A):2929–2936. doi: 10.1016/j.bbamcr.2015.09.003

Figure 3.

Figure 3

Increase in intracellular NAD+ level partially contributes to NAM-induced Sirt1 upregulation. HepG2 cells were treated with NAM at 5 mM for 8 hours with/without 2-hour pretreatment with either FK866, a specific inhibitor of Nampt, or NMN, a direct product of Nampt-catalyzed reaction from NAM in the salvage pathway. A. the de novo pathway, which uses tryptophan as the precursor, and the salvage pathway, which utilizes NAM as the precursor, for NAD+ biosynthesis. Nampt: nicotinamide phophoribosyltransferase, the rate-limiting enzyme of salvage pathway. B. The inhibition of Nampt via FK866 prevents NAM-induced NAD+ increase, which is recovered by NMN supplementation. C: FK866 partially prevents NAM-induced Sirt1 upregulation. All values are denoted as means ± SD from three or more independent studies. Bars with different letters differ significantly (p < 0.05).