Fig 1: Dysregulated NAD+homeostasis in livers of glycine N-methyltransferase knockout mice.A: A schematic representation of select metabolites and enzymes associated with NAD+ synthesis, salvage, and utilization. B-D: Liver metabolites related to redox state in wildtype (WT) and glycine N-methyltransferase deficient (KO) mice; NAD+, NADH, and the NAD+-to-NADH ratio (nmol•g liver wt-1; n = 8–9 per genotype). E: Liver nicotinamide N-methyltransferase (NNMT) as determined by immunoblotting with a representative immunoblot (n = 7 per genotype). F: Liver phosphorylated histone H2AX variant (?H2AX) as determined by immunoblotting with a representative immunoblot (n = 7–8 per genotype). G: Liver poly(ADP-ribose) polymerase 1 (PARP1) as determined by immunoblotting with a representative immunoblot (n = 8 per genotype). H: Liver ADP-ribose (nmol•g liver wt-1; n = 9 per genotype). I: Liver tryptophan (nmol•g liver wt-1; n = 8–9 per genotype). J: Liver tryptophan 2,3-dioxygenase (TDO) as determined by immunoblotting with a representative immunoblot (n = 7 per genotype). K: Liver unconventional prefoldin RPB5 interactor (URI) as determined by immunoblotting with a representative immunoblot (n = 6–7 per genotype). All data are from eight-hour fasted, male mice at 44 weeks of age. Data are mean ± SEM. *p < 0.05 vs. WT.