Obesity is caused by an imbalance between calorie intake and energy expenditure, leading to excessive adipose tissue accumulation. Nicotinamide adenine dinucleotide (NAD+ ) is an important molecule in energy and signal transduction, and NAD+ supplementation therapy is a new treatment for obesity in recent years. Liver kinase B1 (LKB1) is an energy metabolism regulator. The relationship between NAD+ and LKB1 has only been studied in the heart and has not yet been reported in obesity. Nicotinamide mononucleotide (NMN), as a direct precursor of NAD+ , can effectively enhance the level of NAD+ . In the current study, we showed that NMN intervention altered body composition in obese mice, characterized by a reduction in fat mass and an increase in lean mass. NMN reversed high-fat diet-induced blood lipid levels then contributed to reducing hepatic steatosis. NMN also improved glucose tolerance and alleviated adipose tissue inflammation. Moreover, our data suggested that NMN supplementation may be depends on the NAD+ /SIRT6/LKB1 pathway to regulate brown adipose metabolism. These results provided new evidence for NMN in obesity treatment.
Keywords: LKB1; NAD+; SIRT6; adipose tissue; diet-induced obesity; nicotinamide mononucleotide.
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