Spermidine ameliorates high-fat diet-induced hepatic steatosis and adipose tissue inflammation in preexisting obese mice

Aims: The therapeutic effects of spermidine on preexisting obese mice have been not fully elucidated. In this study, we assessed the anti-obesity impact of spermidine on high-fat diet (HFD)-induced obese mice. Main methods: C57BL/6J mice were fed a HFD for 16 weeks to induce obesity, and then treated with or without spermidine via drinking water for additional 8 weeks. The contributions of spermidine in regulating obesity phenotypes and metabolic syndrome were further evaluated. Key findings: Spermidine administration lowered fat mass and plasma lipid profile in HFD-induced obese mice without affecting body weight. In addition, spermidine attenuated hepatic steatosis by regulating lipid metabolism and enhancing antioxidant capacity. Moreover, spermidine reduced adipose tissue inflammation by decreasing inflammatory cytokine and chemokines expression, and these results might contributed to the enhanced thermogenic gene expression in brown adipose tissue. Furthermore, spermidine treatment enhanced gut barrier function by up-regulating tight junction- and mucin-related gene expression. Significance: Spermidine-mediated protective impacts involve the regulation of lipid metabolism, inflammation response, gut barrier function and thermogenesis. These findings demonstrate that spermidine has potentials in treating obesity.

Automated summary

Spermidine administration can reduce fat mass and plasma lipid profile in HFD-induced obese mice, improve hepatic steatosis, reduce adipose tissue inflammation, and enhance gut barrier function. Additionally, spermidine treatment also enhances thermogenic gene expression in brown adipose tissue.