·To investigate the effects of nicotinamide mononucleotide (NMN) on metabolism in aging mice.

·Seventy C57BL/6N male mice were randomly divided into 5 groups by using a table of random numbers. They were the control group, the premature aging model group, the aging model group, the intervention group Ⅰand the intervention group Ⅱ. Each group contained 14 mice. Except the control group, D-galactose (D-gal) (150 mg/kg) was subcutaneously injected into the napes of mice in the other 4 groups to establish the aging model of mice. NMN (300 mg/kg) was given to the intervention group Ⅰ and the intervention group Ⅱ by intragastric administration at the same time, and the other groups were given the same amount of distilled water, once a day, for 6 weeks in the premature aging model group and the intervention group Ⅰ, and for 12 weeks in the aging model group and the intervention group Ⅱ. The control group was given the same amount of normal saline and distilled water, once a day, for 6 weeks. Six weeks after modeling, the energy metabolism levels of the mice in the control group, the premature aging model group and the intervention group Ⅰ were detected, including respiratory metabolism, activity level and energy consumption. The organ indexes of thymus, spleen, liver and kidney were calculated. The glucose tolerance and insulin sensitivity were measured. In addition, the content of superoxide dismutase (SOD) and the activities of glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in the serum and liver tissue were detected. Twelve weeks after modeling, the above indexes were detected in the aging model group and the intervention group Ⅱ.

·Compared with the control group, the thymus index (P=0.035, P=0.000) and renal index (P=0.009, P=0.002) of the model groups were significantly decreased. The O₂ consumption (P=0.018, P=0.000), CO₂ exhalation (P=0.044, P=0.003), energy consumption (P=0.010, P=0.001) and activity ability (both P=0.000) of the premature aging model group and the aging model group were significantly decreased at night. The insulin sensitivity was significantly reduced (P=0.012, P=0.011). The activities of SOD (P=0.002, P=0.001) and GSH-Px (P=0.001, P=0.011) in serum were significantly decreased and the content of MDA in serum was significantly increased (both P=0.000). The decline of energy metabolism levels, thymus and kidney indexes and antioxidant index verified the success of D-gal aging model. Compared with the premature aging model group, the intervention group Ⅰ had no significant difference in respiratory metabolism, energy consumption, glucose tolerance, insulin sensitivity and other indicators (all P>0.05). But in the intervention group Ⅰ, the activity ability was significantly improved (P=0.022), the activities of SOD (P=0.026) and GSH-Px (P=0.006) in serum were significantly increased, and the MDA content in serum was significantly decreased (P=0.011). Compared with the aging model group, the O₂ consumption (P=0.045), CO₂ exhalation (P=0.030), activity ability (P=0.049) and energy consumption (P=0.043) in the intervention group Ⅱ were significantly increased at night. Compared with the aging model group, the impaired glucose tolerance was improved (P=0.030), the insulin sensitivity was increased (P=0.010)in the intervention group Ⅱ, the activity of SOD in serum was significantly increased (P=0.046), and the MDA content in serum and liver tissue was significantly decreased (P=0.000). There was no significant difference in the activity of GSH-Px in serum and liver tissue between the two groups (P>0.05).

·NMN can improve the metabolic level of aging mice to a certain extent, and its mechanism may be related to improving the antioxidant capacity of the body.