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Ligilactobacillus Salivarius LCK11 Prevents Obesity by Promoting PYY Secretion to Inhibit Appetite and Regulating Gut
Cong Liang1, Xiao-Hong Zhou2, Yue-Hua Jiao3
1School of Chemistry and Chemical Engineering, Harbin Institute of Technology, Harbin, 150010, China.
Scope:
Obesity is a common disease worldwide and there is an urgent need for strategies to preventing obesity.
Methods And Results:
The anti-obesity effect and mechanism of Ligilactobacillus salivarius LCK11 (LCK11) is studied using a C57BL/6J male mouse model in which obesity is induced by a high-fat diet (HFD). Results show that LCK11 can prevent HFD-induced obesity, reflected as inhibited body weight gain, abdominal and liver fat accumulation and dyslipidemia. Analysis of its mechanism shows that on the one hand, LCK11 can inhibit food intake through significantly improving the transcriptional and translational levels of peptide YY (PYY) in the rectum, in addition to the eventual serum PYY level; this is attributed to the activation of the toll-like receptor 2/nuclear factor-κB signaling pathway in enteroendocrine L cells by the peptidoglycan of LCK11. On the other hand, LCK11 supplementation effectively reduces the Firmicutes/Bacteroidetes ratio and shifts the overall structure of the HFD-disrupted gut microbiota toward that of mice fed on a low-fat diet; this also contributes to preventing obesity.
Conclusion:
LCK11 shows the potential to be used as a novel probiotic for preventing obesity by both promoting PYY secretion to inhibit food intake and regulating gut microbiota.
Insights
Ligilactobacillus salivarius LCK11 prevents obesity by reducing food intake and improving gut microbiota. This novel probiotic shows potential for managing diet-induced obesity and related metabolic disorders.
Area of Science:
- Microbiology
- Nutrition Science
- Gastroenterology
Background:
- Obesity is a prevalent global health issue requiring effective prevention strategies.
- High-fat diets (HFD) disrupt gut microbiota and contribute to obesity and metabolic dysfunction.
Purpose of the Study:
- To investigate the anti-obesity effects of Ligilactobacillus salivarius LCK11.
- To elucidate the mechanisms underlying LCK11's impact on HFD-induced obesity.
Main Methods:
- Utilized a C57BL/6J male mouse model fed a high-fat diet to induce obesity.
- Administered Ligilactobacillus salivarius LCK11 and assessed its effects on body weight, fat accumulation, and lipid profiles.
- Analyzed molecular mechanisms including peptide YY (PYY) regulation and gut microbiota composition.
Main Results:
- LCK11 significantly inhibited HFD-induced body weight gain, abdominal and liver fat accumulation, and dyslipidemia.
- LCK11 enhanced PYY expression and secretion by activating the toll-like receptor 2/nuclear factor-κB pathway in enteroendocrine L cells, reducing food intake.
- LCK11 modulated gut microbiota, decreasing the Firmicutes/Bacteroidetes ratio and restoring microbial balance.
Conclusions:
- Ligilactobacillus salivarius LCK11 demonstrates significant anti-obesity properties.
- LCK11 acts by promoting PYY secretion to suppress appetite and by re-regulating gut microbiota composition.
- LCK11 holds promise as a novel probiotic for obesity prevention and management.
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