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. Author manuscript; available in PMC: 2022 Jun 25.
Published in final edited form as: Circ Res. 2021 Apr 30;129(1):114–130. doi: 10.1161/CIRCRESAHA.120.317943

Figure 7.

Figure 7.

Endogenous Nampt prevents HFD-induced diastolic dysfunction and oxidative stress.

(A) Body weights in wild type and Nampt+/− mice under HFD feeding conditions. (B) Blood glucose in wild type and Nampt+/− mice under HFD feeding conditions (C) HFD-induced Nampt expression is inhibited in Nampt+/− mice. NS: Non-specific band. (D) HFD-induced diastolic dysfunction is exacerbated in Nampt+/− mice. (E) Endogenous Nampt maintains NAD(H). (F) Endogenous Nampt maintains NADP. (G) Neither Nampt knockdown nor HFD significantly affects the level of NADK and G6PD. (H) Nampt knockdown promotes HFD-induced inhibition of Trx1 substrates. Heart lysates were prepared from WT and Nampt+/− mice after 3 months of HFD consumption. Western blot analyses were performed with indicated antibodies. Statistical significance was determined with ANOVA (C, E (NADH), F (NADPH, NADP+NADPH, NADPH/NADP), G, H (NADK/Tubulin, G6PD/Tubulin, PrdxSO3H/Prdx1, P-mTOR/mTOR. P-S6K/S6K, P-AMPKα/AMPKα, P-ACC/ACC, Dityrosine/Tubulin and P-IKK/IKK), repeated measures ANOVA (A, B) and the Kruskal-Wallis test (D, E (NAD, NAD+NADH, NAD/NADH), F (NADP) and H (Trx1/Tubulin and TLR4/Tubulin).