Bacillus licheniformis Zhengchangsheng® Inhibits Obesity by Regulating the AMP-Activated Protein Kinase Signaling Pathway

As a metabolic syndrome, obesity has become a global public health problem. Bacillus licheniformis has been shown to inhibit obesity by regulating the gut microbiota, but the underlying mechanism of its therapeutic effect is still unknown. In this study, the anti-obesity mechanism of Bacillus licheniformis Zhengchangsheng (R) was investigated by examining a high-fat diet-induced obesity mouse model. Our results showed that Bacillus licheniformis Zhengchangsheng (R) significantly decreased body weight gain and fat accumulation, serum lipid profiles, and proinflammatory cytokine levels and improved glucose and lipid metabolism in obese mice. Furthermore, compared with those of high-fat diet-fed mice, Bacillus licheniformis Zhengchangsheng (R) treatment also inhibited nuclear factor-kappa B activation, increased phosphorylated AMP-activated protein kinase activation in the liver, and regulated the expression of genes associated with lipid metabolism. These results indicated that Bacillus licheniformis Zhengchangsheng (R)-induced obesity inhibition could occur by activating the AMP-activated protein kinase signaling pathway. Thus, our results suggested that Bacillus licheniformis Zhengchangsheng (R) has the potential to treat obesity and related metabolic diseases in the clinic.

Automated summary

Bacillus licheniformis Zhengchangsheng (R) has been shown to inhibit obesity by regulating gut microbiota in obese mice, leading to improved body weight, fat accumulation, serum lipid profiles, inflammatory cytokines, and glucose and lipid metabolism. Additionally, it activates the AMP-activated protein kinase pathway, suggesting its potential in treating obesity and related metabolic diseases.