Li Guanghui, Cheong Kit-Leong, He Yunhua, Liew Ahluk, Huang Jiaxuan, Huang Chen, Zhong Saiyi, Sathuvan Malairaj
Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang 524088, China.
Guangdong Province Engineering Laboratory for Marine Biological Products, Zhanjiang 524088, China.
Foods. 2025 Aug 1;14(15):2708. doi: 10.3390/foods14152708.
Although pulp residues polysaccharides (HPPP) have shown potential in improving metabolic disorders and intestinal barrier function, the mechanism by which they exert their effects through regulating O-glycosylation modifications in the mucus layer remains unclear. Therefore, this study established a HFD-induced obese colitis mouse model ( = 5 per group) and combined nano-capillary liquid chromatography-tandem mass spectrometry (nanoLC-MS/MS) technology to quantitatively analyze the dynamic changes in O-glycosylation. Additionally, through quantitative O-glycosylation proteomics and whole-proteome analysis, we identified 155 specifically altered O-glycosylation sites in colon tissue, with the glycosylation modification level of the MUC2 core protein increased by approximately 2.1-fold. The results indicate that HPPP alleviates colonic mucosal damage by regulating interactions between mucus O-glycosylation. Overall, we demonstrated that HPPP increases HFD-induced O-glycosylation sites, improves intestinal mucosal structure in obese mice, and provides protective effects against obesity-induced intestinal mucosal damage.
尽管果肉残渣多糖(HPPP)在改善代谢紊乱和肠道屏障功能方面已显示出潜力,但其通过调节黏液层中的O-糖基化修饰发挥作用的机制仍不清楚。因此,本研究建立了高脂饮食诱导的肥胖性结肠炎小鼠模型(每组n = 5),并结合纳升毛细管液相色谱-串联质谱(nanoLC-MS/MS)技术对O-糖基化的动态变化进行定量分析。此外,通过定量O-糖基化蛋白质组学和全蛋白质组分析,我们在结肠组织中鉴定出155个特异性改变的O-糖基化位点,MUC2核心蛋白的糖基化修饰水平增加了约2.1倍。结果表明,HPPP通过调节黏液O-糖基化之间的相互作用减轻结肠黏膜损伤。总体而言,我们证明HPPP增加了高脂饮食诱导的O-糖基化位点,改善了肥胖小鼠的肠道黏膜结构,并对肥胖诱导的肠道黏膜损伤具有保护作用。
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