Bacillus licheniformis Zhengchangsheng® Inhibits Obesity by Regulating the AMP-Activated Protein Kinase Signaling Pathway.
AMPK
Bacillus licheniformis
Lipid metabolism
NF-κB
Obesity
Journal
Probiotics and antimicrobial proteins
ISSN: 1867-1314
Titre abrégé: Probiotics Antimicrob Proteins
Pays: United States
ID NLM: 101484100
Informations de publication
Date de publication:
12 2021
12 2021
Historique:
accepted:
19
04
2021
pubmed:
7
5
2021
medline:
13
1
2022
entrez:
6
5
2021
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 33954883
doi: 10.1007/s12602-021-09792-6
pii: 10.1007/s12602-021-09792-6
doi:
Substances chimiques
AMP-Activated Protein Kinases
EC 2.7.11.31
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1658-1667Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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