| Literature DB >> 33954883 |
Xiaojie Lu1, Yue Jing1, Xiaofei Zhou1, Naisheng Zhang1, Jiandong Tai2, Yongguo Cao3.
Abstract
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.Entities:
Keywords: AMPK; Bacillus licheniformis; Lipid metabolism; NF-κB; Obesity
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Year: 2021 PMID: 33954883 DOI: 10.1007/s12602-021-09792-6
Source DB: PubMed Journal: Probiotics Antimicrob Proteins ISSN: 1867-1306 Impact factor: 4.609