Study on the Regulatory Mechanism of Niacin Combined with B. animalis F1-7 in Alleviating Alcoholic Fatty Liver Disease by Up-Regulating GPR109A

This study aimed to investigate the effects of niacin combined with F1-7 on the improvement of alcoholic fatty liver disease (AFLD) in mice and its potential regulatory mechanism. A total of 75 8-week-old male C57BL/6N mice were acclimated for one week and randomly divided into five groups: control group, alcohol model group (AFLD), niacin intervention group (NA), F1-7 intervention group (F1-7), and niacin combined with F1-7 intervention group (NF). The experiment lasted for 8 weeks. The results showed that all intervention groups could effectively reduce the serum lipid levels and inflammatory response of mice induced by alcohol to varying degrees. The immunofluorescence analysis showed that the GPR109A in the liver and intestine of the NF group was significantly enhanced compared with the other groups. Niacin combined with F1-7 better restored the gut microbiota. Meanwhile, each intervention group could increase their levels of SCFAs. Among them, the combination group increased the levels of acetic acid and butyric acid more significantly than the other two groups. The Spearman's correlation analysis of gut microbiota and SCFAs showed that , , and were positively correlated with changes in SCFAs, while , , and were negatively correlated. Niacin combined with F1-7 better regulated the gut microbial balance and increased the SCFAs in mice with alcoholic steatohepatitis. The mechanism was related to the activation of the target GPR109A, which regulates the key proteins involved in lipid synthesis and -oxidation to improve lipid metabolic disorders.