The objective of this study was to elucidate the effect of intestinal Akkermansia muciniphila on fatty liver disease. Five-week-old C57BL/6N mice were administered either phosphate buffer saline (PBS, control) or A. muciniphila at 10⁸-10⁹ CFU/mL, and were fed either a 45% fat diet (HFD, high-fat diet) or a 10% fat diet (ND) for 10 weeks. After 10 weeks, the mice were euthanized, and the blood and tissue samples, including adipose tissue, caecum, liver, and brain, were immediately collected. Biochemical and histological analyses were conducted and the expression levels of related factors were compared to determine the anti-obesity effects of Akkermansia muciniphila. The gut microbiome was analyzed in fecal samples. Oral administration of A. muciniphila significantly (p < 0.05) lowered serum triglyceride (TG), and alanine aminotransferase (ALT) levels in obese mice. Compared to the non-A. muciniphila-treated group, the expression of SREBP (regulator of TG synthesis in liver tissue) was decreased in the A. muciniphila-treated group. The expression of IL-6 in the liver of obese mice was decreased following the administration of A. muciniphila. Furthermore, alterations in the Firmicutes to Bacteroidetes ratio and decrease in bacterial diversity caused by the HFD were restored upon the administration of A. muciniphila. These results indicate that A. muciniphila prevents fatty liver disease in obese mice by regulating TG synthesis in the liver and maintaining gut homeostasis.

Importance This study investigated the effect of Akkermansia muciniphila on fatty liver disease. Though some researches about effects of A. muciniphila on host health were published, the study on relation between A. muciniphila administration and fatty liver as well as changes of gut microbiota have not been conducted. In this study we specifically focused on composition of gut microbiota, and also demonstrate gene expression levels, regulating fat synthesis and inflammation in the liver.

这项研究的目的是阐明肠黏膜阿克曼氏菌对脂肪肝的影响。给五周大的C57BL / 6N小鼠以10 ⁸ -10 ⁹ CFU / mL的磷酸盐缓冲盐水（PBS，对照）或黏液曲霉（A. muciniphila）给药，并饲喂45％的脂肪饮食（HFD，高脂饮食） ）或10％的脂肪饮食（ND），持续10周。10周后，对小鼠实施安乐死，并立即收集血液和组织样本，包括脂肪组织，盲肠，肝脏和大脑。进行了生化和组织学分析，并比较了相关因子的表达水平，以确定粘蛋白阿克曼（Akkermansia muciniphila）的抗肥胖作用。在粪便样品中分析了肠道微生物组。口服A. muciniphila可以显着降低（p <0.05）肥胖小鼠的血清甘油三酸酯（TG）和丙氨酸氨基转移酶（ALT）的水平。与非A. muciniphila治疗组相比，SREBP（肝组织中TG合成的调节剂）的表达在A. muciniphila治疗组中降低。给予粘液曲霉后，肥胖小鼠肝脏中IL-6的表达降低。此外，HFD引起的硬菌对拟杆菌比率的改变和细菌多样性的降低在施用HFD后得以恢复。A. muciniphila。这些结果表明黏液曲霉可通过调节肝脏中的TG合成并维持肠道稳态来预防肥胖小鼠的脂肪肝疾病。

重要性这项研究调查了Akkermansia muciniphila对脂肪肝疾病的影响。尽管已经发表了关于嗜A.muciniphila对宿主健康的影响的一些研究，但尚未进行关于嗜A. muciniphila施用与脂肪肝之间关系以及肠道菌群变化的研究。在这项研究中，我们特别关注肠道菌群的组成，并证明基因表达水平，调节脂肪合成和肝脏炎症。