在这项研究中,我们研究了海带多糖(岩藻依聚糖)对脂质代谢的调节作用。采用高糖高脂饮食联合链脲佐菌素建立糖尿病(DM)大鼠模型。记录实验期间大鼠体重和血糖水平的变化。在实验结束之前,采用全自动生化分析仪检测空腹血糖(FBG),血清脂质含量,和胰岛素含量,并计算胰岛素抵抗指数。油红O染色用于检测肝脏中的脂质沉积。H&E染色,Masson染色,PASM染色观察肝脏病理结构改变。采用16sRNA测序和靶向代谢组学方法检测肠道菌群和胆汁酸含量。结果表明,岩藻依聚糖能够抑制DM大鼠的体重减轻,降低甘油三酯(TG)的含量,胆固醇(TC),和血清低密度脂蛋白(LDL-C)。油红O染色显示岩藻依聚糖处理后肝脏脂肪积累减少。16sRNA测序表明,岩藻依聚糖增加了拟杆菌的丰度,弯曲杆菌,梭菌,γ变形杆菌,否认,和Verrucomicrobi。岩藻依聚糖还增加了次级胆汁酸的分泌(Nor-DCA,TLCA,β-UDCA)和减轻脂质代谢紊乱。岩藻依聚糖抑制α-SMA的表达,而FXR和TGR5的表达被促进。岩藻聚糖通过调节FXR和TGR5的表达并作用于肠道菌群-胆汁酸轴,在调节脂质代谢方面表现出良好的活性。
In this study, we examined the effect of Laminaria japonica polysaccharide (fucoidan) on the regulation of lipid metabolism. A rat model of diabetes mellitus (DM) was established by a high-sugar and high-fat diet combined with streptozotocin. Changes in the rats\' body weight and blood glucose level during the experiment were recorded. Before the end of the experiment, an automatic biochemical analyzer was used to detect the fasting blood glucose (FBG), lipid content in serum, and insulin content, and calculate the insulin resistance index. Oil red O staining was used to detect lipid deposition in the liver. H&E staining, Masson staining, and PASM staining were used to observe the pathological structural changes in the liver. 16 s RNA sequencing and targeted metabolomics were used to detect intestinal microbiota and bile acid content. The results showed that fucoidan was able to inhibit weight loss in the DM rats and reduce the content of triglycerides (TG), cholesterol (TC), and low-density lipoprotein (LDL-C) in serum. Oil red O staining showed a decrease in liver fat accumulation after fucoidan treatment. 16 s RNA sequencing demonstrated that fucoidan increased the abundance of Bacteroidia, Campylobacteria, Clostridia, Gammaproteobacteria, Negativicutes, and Verrucomicrobi. Fucoidan also increased the secretion of secondary bile acids (Nor-DCA, TLCA, β-UDCA) and alleviated lipid metabolism disorders. The expression of α-SMA was inhibited by fucoidan, whereas the expression of FXR and TGR5 was promoted. Fucoidan shows good activity in regulating lipid metabolism by regulating the expression of FXR and TGR5 and acting on the intestinal flora-bile acid axis.