Dietary Supplementation of Auricularia auricula-judae Polysaccharides Alleviate Nutritional Obesity in Mice via Regulating Inflammatory Response and Lipid Metabolism

The incidence of lipid metabolism disorder and obesity that is caused by high-calorie diets is increasing year by year, which has become an urgent global health problem. This study was performed to explore the intervention effects of polysaccharides that were extracted from Auricularia auricula-judae resources in the Qinba Mountain area on nutritional obesity in C57BL/6J mice that was induced by high fat and high fructose diets (HFFD) and to investigate their underlying molecular mechanisms. The results showed that dietary supplementation of Auricularia auricula-judae polysaccharides (AAP) significantly improved mice's insulin resistance state, altered serum lipid metabolites, and slowed down body weight gain that was induced by HFFD. In addition, AAP supplementation decreased inflammatory factor levels and alleviated liver histomorphology changes. Furthermore, AAP down-regulated liver adipogenic-related gene expressions, suppressed cholesterol synthesis-related gene levels, up-regulated fatty acid beta-oxidation-related gene expressions, and promoted cholesterol efflux-related gene expressions, thus improving mice hepatic lipid metabolism homeostasis. Moreover, the intervention effects were closely related to mitochondrial function. These results provide a scientific basis for the further development and utilization of Auricularia auricula-judae resources in the Qinba Mountain area.

Automated summary

This study investigated the intervention effects and underlying molecular mechanisms of polysaccharides extracted from Auricularia auricula-judae resources in the Qinba Mountain area on nutritional obesity induced by high fat and high fructose diets (HFFD) in C57BL/6J mice. The results demonstrated that dietary supplementation of Auricularia auricula-judae polysaccharides significantly improved insulin resistance, altered serum lipid metabolites, and slowed down body weight gain induced by HFFD. The intervention effects were associated with the regulation of adipogenic-related gene expressions, cholesterol synthesis-related gene levels, fatty acid beta-oxidation-related gene expressions, and cholesterol efflux-related gene expressions in the liver, indicating improvements in hepatic lipid metabolism homeostasis. Furthermore, these effects were closely related to mitochondrial function.