高脂肪饮食(HFDs)塑造肠道微生物组并促进肥胖,炎症,和肝脏脂肪变性.鱼和大豆是健康饮食的一部分;然而,这些脂肪的影响,在没有蔗糖的情况下,肠道微生物菌群失调及其与肝脏脂肪变性的关系尚不清楚。这里,我们调查了无蔗糖大豆油和鱼油为基础的高脂肪饮食(HFDs)(SF-Soy-HFD和SF-Fish-HFD,分别)关于肠道生态失调,肥胖,脂肪变性,肝脏炎症,和胰岛素抵抗。C57BL/6小鼠饲喂这些HFDs24周。两种饮食对肝脏和总体重具有相当的影响。但是对肠道内容物的16S-rRNA测序显示在不同的分类水平上诱导了肠道生态失调。微生物群落被清晰地分离,显示两个HFDs之间的不同生态失调。与SF-Fish-HFD对照组相比,SF-Soy-HFD组的拟杆菌丰度增加,Firmicutes,和去铁杆菌,但是Verrucomicrobia的丰度较低。SF-Soy-HFD组(3.11)的梭菌/细菌(C/B)比率高于SF-Fish-HFD组(2.5)。相反,SF-Soy-HFD组的Verrucobiacae/S24_7(也称为Muribaculaceae家族)比率(0.02)低于SF-Fish-HFD组(0.75)。SF-Soy-HFD组与S24_7,梭菌,Allobaculum,科氏杆菌科,Adlercreutzia,Christensenellaceae,乳球菌,和螺旋体,但与阿克曼西亚的丰度较低有关,保持肠道屏障的完整性。SF-Soy-HFD组中的肠道微生物群预测了与脂肪肝和炎症途径相关的宿主基因的关联。喂食SF-Soy-HFD的小鼠出现肝脏脂肪变性,并显示与从头脂肪生成相关的基因转录水平增加(Acaca,Fasn,与SF-Fish-HFD组相比,Scd1,Elovl6)和胆固醇合成(Hmgcr)途径。在脂肪摄取基因(Cd36和Fabp1)的表达中没有观察到差异。SF-Soy-HFD组中脂肪流出基因(Mttp)的表达降低。此外,肝脏炎症标志物(Tnfa和Il1b)在SF-Soy-HFD喂养的小鼠中显著表达。总之,SF-Soy-HFD喂养诱导小鼠肠道菌群失调,导致脂肪变性,肝脏炎症,和受损的葡萄糖稳态。
High-fat diets (HFDs) shape the gut microbiome and promote obesity, inflammation, and liver
steatosis. Fish and soybean are part of a healthy diet; however, the impact of these fats, in the absence of sucrose, on gut microbial dysbiosis and its association with liver
steatosis remains unclear. Here, we investigated the effect of sucrose-free soybean oil-and fish oil-based high fat diets (HFDs) (SF-Soy-HFD and SF-Fish-HFD, respectively) on gut dysbiosis, obesity,
steatosis, hepatic inflammation, and insulin resistance. C57BL/6 mice were fed these HFDs for 24 weeks. Both diets had comparable effects on liver and total body weights. But 16S-rRNA sequencing of the gut content revealed induction of gut dysbiosis at different taxonomic levels. The microbial communities were clearly separated, showing differential dysbiosis between the two HFDs. Compared with the SF-Fish-HFD control group, the SF-Soy-HFD group had an increased abundance of Bacteroidetes, Firmicutes, and Deferribacteres, but a lower abundance of Verrucomicrobia. The Clostridia/Bacteroidia (C/B) ratio was higher in the SF-Soy-HFD group (3.11) than in the SF-Fish-HFD group (2.5). Conversely, the Verrucomicrobiacae/S24_7 (also known as Muribaculaceae family) ratio was lower in the SF-Soy-HFD group (0.02) than that in the SF-Fish-HFD group (0.75). The SF-Soy-HFD group had a positive association with S24_7, Clostridiales, Allobaculum, Coriobacteriaceae, Adlercreutzia, Christensenellaceae, Lactococcus, and Oscillospira, but was related to a lower abundance of Akkermansia, which maintains gut barrier integrity. The gut microbiota in the SF-Soy-HFD group had predicted associations with host genes related to fatty liver and inflammatory pathways. Mice fed the SF-Soy-HFD developed liver
steatosis and showed increased transcript levels of genes associated with de novo lipogenesis (Acaca, Fasn, Scd1, Elovl6) and cholesterol synthesis (Hmgcr) pathways compared to those in the SF-Fish-HFD-group. No differences were observed in the expression of fat uptake genes (Cd36 and Fabp1). The expression of the fat efflux gene (Mttp) was reduced in the SF-Soy-HFD group. Moreover, hepatic inflammation markers (Tnfa and Il1b) were notably expressed in SF-Soy-HFD-fed mice. In conclusion, SF-Soy-HFD feeding induced gut dysbiosis in mice, leading to
steatosis, hepatic inflammation, and impaired glucose homeostasis.