Fucoidan derived from Saccharina japonica: structural characterization and amelioration of high-fat-diet induced obesity in male C57BL/6 J mice via modulating the gut microbiota and lipid metabolites.

Fucoidan has great potential for the prevention and treatment of obesity. This study aimed to determine the detailed structure of two fucoidan fractions (LF3-1 and LF4-1) from Saccharina japonica (S. japonica) and its mechanism for treating obesity. LF3-1 and LF4-1, with a molecular weight of 305.3 kDa and 182.1 kDa, respectively, were obtained from S. japonica. The backbone of LF3-1 consisted of →1,3)-α-L-Fucp4S-(1 → and →1,3)-β-D-Galp6S-(1→, branched with α-L-Fucp, β-D-Galp, and β-D-Manp. LF4-1's backbone consisted of →1,3)-α-L-Fucp4S-(1 → and →1,6)-β-D-Galp3S-(1→, branched with α-L-Fucp, β-D-Galp, and β-D-Manp. Over 24 weeks in high-fat-diet-fed C57BL/6 J mice, a mixture of LF3-1 and LF4-1 (100 and 300 mg/kg/d FUC) effectively reduced body weight and insulin resistance, ameliorated dyslipidemia, protected the intestinal barrier integrity, up-regulated Ucp-1, Prdm16 and Pgc-1α expression to inhibit fat accumulation, up-regulated Ppar-α, Ppar-γ, and Cpt-1 expression and down-regulation Fas, Lxr, and Srebp-1c expression to regulate lipid metabolism, and down-regulated expression of Tnf-α, Il-6, Il-1β, and Mcp-1 to ameliorate inflammation. In addition, FUC increased the abundance of Bacteroidetes and Lactobacillus. Lipid metabolomics analysis showed that Erysipelatoclostridium, Lachnoclostridium, Ruminococcaceae_UCG-014, and Staphylococcus may be involved in regulating sphingosine (SPH). This study revealed the structure properties and the potential of the application of FUC in the amelioration of obesity.