Current evidence suggests that high fructose intake results in gut dysbiosis, leading to endotoxemia and NAFLD onset. Thus, the hypothesis of the study was that an enhanced Proteobacteria proportion in the cecal microbiota could be the most prominent trigger of NAFLD through enhanced endotoxin (LPS) in adult high-fructose-fed C57BL/6 mice. Male C57BL/6 mice received a control diet (n = 10, C: 76% of energy as carbohydrates, 0% as fructose) or high-fructose diet (n = 10, HFRU: 76% of energy as carbohydrate, 50% as fructose) for 12 weeks. Outcomes included biochemical analyses, 16S rDNA PCR amplification, hepatic stereology, and RT-qPCR. The groups showed similar body masses during the whole experiment. However, the HFRU group showed greater water intake and blood pressure than the C group. The HFRU group showed a significantly lower amount of Bacteroidetes and a predominant rise in Proteobacteria, implying increased LPS. The HFRU group also showed enhanced de novo lipogenesis (Chrebp expression), while beta-oxidation was decreased (Ppar-alpha expression). These results agree with the deposition of fat droplets within hepatocytes and the enhanced hepatic triacylglycerol concentrations, as observed in the photomicrographs, where the HFRU group had a higher volume density of steatosis than the C group. Thus, we confirmed that a rise in the Proteobacteria phylum proportion was the most prominent alteration in gut-liver axis-induced hepatic steatosis in HFRU-fed C57BL/6 mice. Gut dysbiosis and fatty liver were observed even in the absence of overweight in this dietary adult mouse model.

目前的证据表明，高果糖摄入会导致肠道菌群失调，导致内毒素血症和 NAFLD 发病。因此，该研究的假设是，在成年高果糖喂养的 C57BL/6 小鼠中，盲肠微生物群中变形菌比例的增加可能是通过增强内毒素 (LPS) 导致 NAFLD 的最显着触发因素。雄性 C57BL/6 小鼠接受对照饮食（n = 10，C：76% 能量为碳水化合物，0% 为果糖）或高果糖饮食（n = 10，HFRU：76% 能量为碳水化合物，50% 为果糖）果糖）12周。结果包括生化分析、16S rDNA PCR 扩增、肝脏体视学和 RT-qPCR。在整个实验过程中，各组的体重相似。然而，HFRU 组的饮水量和血压均高于 C 组。 HFRU 组显示拟杆菌门数量显着降低，变形菌门数量显着增加，这意味着 LPS 增加。 HFRU 组还表现出从头脂肪生成增强（ Chrebp表达），而 β-氧化减少（ Ppar-α表达）。这些结果与显微照片中观察到的肝细胞内脂肪滴沉积和肝脏三酰甘油浓度增加一致，其中 HFRU 组的脂肪变性体积密度高于 C 组。因此，我们证实变形菌门比例的增加是 HFRU 喂养的 C57BL/6 小鼠肠肝轴诱导的肝脂肪变性中最显着的改变。即使在这种饮食成年小鼠模型中没有超重的情况下，也观察到肠道菌群失调和脂肪肝。