Figure 2. Nicotinamide mononucleotide (NMN) administration restores NAD⁺ levels in the p32cKO heart.

(A) LC-MS/MS metabolomic analysis of nicotinamide adenine dinucleotide (NAD⁺), nicotinamide (NAD⁺), nicotinamide adenine dinucleotide, reduced form (NADH), nicotinamide adenine dinucleotide monophosphate (NADP⁺), and nicotinamide adenine dinucleotide monophosphate reduced form (NADPH) in heart tissue of 9-mo-old WT and p32cKO mice treated with or without NMN from 2 to 9 mo of age (WT, p32cKO, and p32cKO + NMN: n = 5, WT + NMN: n = 6). NAD⁺ and NADP⁺ show significantly different levels between WT and p32cKO hearts. Data are presented as the mean ± SEM. (B) RNA expression of NAD⁺-synthesizing enzymes in WT and p32cKO hearts under treatment with or without NMN from 2 to 9 mo of age (WT: n = 5, WT + NMN: n = 6, p32cKO and p32cKO + NMN: n = 5). Data are presented as the mean ± SD. (C) Western blot analysis of hypoxia-inducible factor 1α in the heart of WT and p32cKO mice, and of p32cKO mice treated with NMN from 2 to 9 mo of age. Quantification is shown in the right panel (WT and p32cKO: n = 4, p32cKO + NMN: n = 5). **P = 0.0037, *P = 0.0181. GAPDH was used as an internal control. Error bars show the mean ± SD. (A, B, C) Data were analyzed by one-way analysis of variance with Tukey’s multiple comparisons test. *P < 0.05, **P < 0.01, ***P < 0.001.

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