Deng Qihuan, Xiong Shiyi, Wang Wenjun, Zheng Guodong, Xie Jingjing, He Xiaojin, Ye Liang, Yu Lili, Li Jingen
College of Food Science and Engineering, Jiangxi Agricultural University, Nanchang, 330045, China.
Citrus Research Institute, Southwest University, National Citrus Engineering and Technology Research Center, Chongqing, 400712, China.
Curr Res Food Sci. 2025 Jun 1;10:101103. doi: 10.1016/j.crfs.2025.101103. eCollection 2025.
In this study, the effect of Gougunao tea polysaccharide (GTP40) on lipid metabolism in high-fat diet (HFD)-induced hyperlipidemic mice and its core structure were investigated. GTP40 effectively reversed the increase in weights of the liver and adipose tissues induced by HFD. The oxidative stress of the liver was also significantly alleviated following GTP40 intervention. According to the results of Real-Time quantitative Polymerase Chain Reaction (RT-qPCR), the genes associated with lipolysis were upregulated after GTP40 treatment, while lipogenesis-related genes were downregulated. Additionally, a homogeneous polysaccharide (GTP40-5P, obtained by degrading GTP40 for 5 h) with a molecular weight of 27858 Da was fractionated from GTP40 by the partial acid hydrolysis method. GTP40-5P was mainly composed of 62.30 ± 0.70 % neutral sugar, 54.82 ± 0.51 % uronic acid and 2.52 ± 0.74 % protein. The results of methylation and nuclear magnetic resonance (NMR) analysis indicated that the backbone of GTP40-5P was consisted of →4)--D-GalA-(1 → 4)--D-Gal-(1→ units, with the terminal residue -D-Gal-(1→ linked to →3,4)--D-GalA-(1→ at the -3 site, suggesting that it should be classified as homogalacturonan (HG)-type pectin with partial methyl esterification. These findings indicate that GTP40 alleviates lipid metabolism disorders in hyperlipidemic mice primarily the AMPK signaling pathway. Furthermore, the elucidation of the primary structure of Gougunao tea polysaccharide enhances the understanding of the structure-activity relationship.
本研究考察了狗牯脑茶多糖（GTP40）对高脂饮食（HFD）诱导的高脂血症小鼠脂质代谢的影响及其核心结构。GTP40有效逆转了HFD诱导的肝脏和脂肪组织重量增加。GTP40干预后，肝脏的氧化应激也显著减轻。根据实时定量聚合酶链反应（RT-qPCR）结果，GTP40处理后与脂肪分解相关的基因上调，而与脂肪生成相关的基因下调。此外，通过部分酸水解法从GTP40中分离出一种分子量为27858 Da的均匀多糖（GTP40-5P，通过将GTP40降解5小时获得）。GTP40-5P主要由62.30±0.70%的中性糖、54.82±0.51%的糖醛酸和2.52±0.74%的蛋白质组成。甲基化和核磁共振（NMR）分析结果表明，GTP40-5P的主链由→4)--D-半乳糖醛酸-(1→4)--D-半乳糖-(1→单元组成，末端残基-D-半乳糖-(1→在-3位点与→3,4)--D-半乳糖醛酸-(1→相连，表明它应归类为具有部分甲酯化的同型半乳糖醛酸（HG）型果胶。这些发现表明，GTP40主要通过AMPK信号通路减轻高脂血症小鼠的脂质代谢紊乱。此外，对狗牯脑茶多糖一级结构的阐明增强了对结构-活性关系的理解。
