Sirtuins are a group of histone/protein deacetylases that are regulated by changes in the cellular redox state (NAD+/NADH ratio) and increases in nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme for NAD synthesis. Sirtuins have been evaluated intensively because of their apparent role in combating aging (84, 85). SIRT1, the most studied member of this family, responds to overfeeding, starvation, changes in energy expenditure and exercise (13), as well as to adiponectin (54), much as AMPK does, although with somewhat different timing (13). SIRT1 can activate AMPK by deacetylating the upstream kinase LKB1, which promotes LKB1 translocation from the nucleus to the cytosol, where it is activated and in turn phosphorylates and activates AMPK (86–88). Likewise, AMPK can activate SIRT1 by increasing the NAD/NADH ratio or the expression/activity of NAMPT (89). Collectively, these findings suggest the existence of an AMPK-SIRT1 cycle that links the cell’s energy and redox states (13). In addition, AMPK and SIRT1 (and most likely other sirtuins) act on common transcriptional activators and coactivators, including the mitochondrial master regulator PGC1α and members of the FoxO family. Finally, both AMPK and SIRT1 activators can decrease atherosclerosis and prevent diabetes in experimental animals
AMPK by itself will increase NAD+ levels. I wonder how much more? As much as a NAD+ precursor? Enough to reach a more youthful level?