Feng Xiaoyan, Wang Mengqi, Wen Siyue, Hu Liehai, Lan Yuzhi, Xu Hengyi
State Key Laboratory of Food Science and Resource, Nanchang University, 235 Nanjing East Road, Nanchang, 330047, P. R. China.
International Institute of Food Innovation Co., Ltd., Nanchang University, Nanchang, 330200, P. R. China.
Probiotics Antimicrob Proteins. 2024 Oct 10. doi: 10.1007/s12602-024-10373-6.
Mitigating steatosis is essential for delaying the progression of alcoholic liver disease. The effect and mechanism of Lactiplantibacillus plantarum P101 (LP.P101) on alleviating alcohol-induced hepatic lipid accumulation were investigated in our study. The mouse model was constructed by a short-term (10-day)-plus-binge ethanol feeding and gavaged with 10 CFU/mL of LP.P101 daily. Lipid droplet in the liver was significantly reduced by LP.101 intervention on AMPK activation. However, when AMPK was inhibited by dorsomorphin, the levels of related indicators (ALT, TG, etc.) and the expression levels of AMPK and relevant genes in the liver converged to that of the alcohol-fed group. Compared with the alcohol-fed group, LP.P101 reduced the relative abundance of Firmicutes and increased that of Bacteroidetes. Parabacteroides merdae was negatively correlated with lipid accumulation, and unclassified Negativibacillus was negatively associated with AMPK activation. Importantly, LP.P101 modified the compositions of the serum metabolites. The potential biomarker stercobilinogen was positively correlated with AMPK activation and negatively associated with lipid accumulation. This work confirmed that LP.P101 attenuated alcohol-induced hepatic lipid accumulation in mice through AMPK activation, and the alterations in gut microbiota and metabolites may play a significant role on AMPK activation.
减轻脂肪变性对于延缓酒精性肝病的进展至关重要。本研究探讨了植物乳杆菌P101（LP.P101）减轻酒精诱导的肝脏脂质积累的作用及机制。通过短期（10天）加暴饮乙醇喂养构建小鼠模型，每天灌胃10 CFU/mL的LP.P101。LP.101干预通过激活AMPK显著减少了肝脏中的脂滴。然而，当用 dorsomorphin抑制AMPK时，肝脏中相关指标（ALT、TG等）的水平以及AMPK和相关基因的表达水平与酒精喂养组趋同。与酒精喂养组相比，LP.P101降低了厚壁菌门的相对丰度，增加了拟杆菌门的相对丰度。粪副拟杆菌与脂质积累呈负相关，未分类的Negativibacillus与AMPK激活呈负相关。重要的是，LP.P101改变了血清代谢物的组成。潜在生物标志物粪胆原与AMPK激活呈正相关，与脂质积累呈负相关。这项工作证实，LP.P101通过激活AMPK减轻了小鼠酒精诱导的肝脏脂质积累，肠道微生物群和代谢物的改变可能对AMPK激活起重要作用。
