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® was investigated by examining a high-fat diet-induced obesity mouse model. Our results showed that Bacillus licheniformis Zhengchangsheng® 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® treatment also inhibited nuclear factor-κB 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®-induced obesity inhibition could occur by activating the AMP-activated protein kinase signaling pathway. Thus, our results suggested that Bacillus licheniformis Zhengchangsheng® has the potential to treat obesity and related metabolic diseases in the clinic.

作为一种代谢综合征，肥胖已成为全球公共卫生问题。地衣芽孢杆菌已被证明通过调节肠道菌群来抑制肥胖，但其治疗作用的潜在机制仍不清楚。在这项研究中，通过检查高脂饮食诱导的肥胖小鼠模型，研究地衣芽孢杆菌正肠生®的抗肥胖机制。我们的研究结果表明，地衣芽孢杆菌正肠生®显着降低了肥胖小鼠的体重增加和脂肪积累、血清脂质谱和促炎细胞因子水平，并改善了糖脂代谢。此外，与高脂饮食喂养的小鼠相比，地衣芽孢杆菌正畅生®治疗还抑制核因子-κB活化，增加肝脏中磷酸化AMP激活的蛋白激酶活化，并调节与脂质代谢相关的基因表达。这些结果表明，地衣芽孢杆菌Zhengchangsheng®诱导的肥胖抑制可能是通过激活AMP激活的蛋白激酶信号通路来实现的。因此，我们的研究结果表明，地衣芽孢杆菌正肠生®在临床上具有治疗肥胖及相关代谢疾病的潜力。