Journal of the science of food and agriculture · 2023
Lactobacillus coryniformis subsp. torquens T3 alleviates non-alcoholic fatty liver disease via reconstruction of the gut microbiota and redox system.
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Song Wei, Wang Tianyi, Cui Xiaole, Li Lingling, Chen Bing, Li Yanjie, Yue Tianli
Аннотация
BACKGROUND: A high-fat diet (HFD) that induces obesity has become the most common type of diet worldwide, leading to serious global health issues. Obesity is associated with an increased risk of non-alcoholic fatty liver disease (NAFLD). Probiotic supplements have been shown to help alleviate obesity. The present study aimed to investigate the mechanism by which Lactobacillus coryniformis supsp. torquens T3 (T3L) alleviated NAFLD induced by HFD via reconstruction of the gut microbiota and redox system.
RESULTS: The results showed that, compared with the HFD group, T3L inhibited obesity and relieved fat accumulation in the liver of mice with NAFLD. In addition, T3L inhibited liver inflammation and oxidative stress injury in NAFLD mice by regulating the lipopolysaccharide (LPS) inflammatory pathway in the liver. Furthermore, T3L changed the composition of the intestinal flora, reduced the abundance of harmful bacteria in the intestinal tract, enhanced the mechanical function of the intestinal barrier, and increased the short-chain fatty acid contents, thus inhibiting the secondary metabolite LPS, which directly causes liver damage through the portal vein.
CONCLUSION: In summary, T3L ameliorated NAFLD induced by obesity through the liver-gut axis pathway, thus reducing oxidative stress and liver injury. © 2023 Society of Chemical Industry.
RESULTS: The results showed that, compared with the HFD group, T3L inhibited obesity and relieved fat accumulation in the liver of mice with NAFLD. In addition, T3L inhibited liver inflammation and oxidative stress injury in NAFLD mice by regulating the lipopolysaccharide (LPS) inflammatory pathway in the liver. Furthermore, T3L changed the composition of the intestinal flora, reduced the abundance of harmful bacteria in the intestinal tract, enhanced the mechanical function of the intestinal barrier, and increased the short-chain fatty acid contents, thus inhibiting the secondary metabolite LPS, which directly causes liver damage through the portal vein.
CONCLUSION: In summary, T3L ameliorated NAFLD induced by obesity through the liver-gut axis pathway, thus reducing oxidative stress and liver injury. © 2023 Society of Chemical Industry.