Maternal β-Nicotinamide Mononucleotide Supplementation Reduces the IUGR Rate by Improving Mitochondrial Function in...

Metabolic disturbances in late gestation contributes to oxidative stress and mitochondrial dysfunction in the placenta, leading to intrauterine growth retardation (IUGR), all of which are associated with reduced nicotinamide adenine dinucleotide (NAD⁺) levels. This study aimed to investigate the effects of maternal supplementation of β-nicotinamide mononucleotide (NMN), a nutraceutical NAD⁺ precursor, on IUGR rate and its underlying mechanisms. A total of 24 sows were randomly divided into either the control or NMN group, with each sow in the NMN group receiving 0.2 g of NMN per day. The results demonstrated that NMN supplementation significantly reduced the IUGR rate and increased NAD⁺ levels in the placenta of sows. Furthermore, NMN supplements upregulated mRNA and protein expressions of key mitochondrial regulators, such as PGC-1α, declined oxidative stress and apoptosis, and improved lipid metabolism in the placenta. These effects were linked to the upregulation of p-AMPK and the downregulation expression of p-mTOR. Taken together, this study indicates that maternal NMN supplementation reduces the IUGR rate by improving mitochondria function, enhancing lipid metabolism, and declining oxidative stress in the placenta.