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纸残留物多糖减轻高脂肪饮食诱导的肥胖症通过调节肠道粘液分泌和糖化

Guanghui Li^1,2,3,4,5, Kit-Leong Cheong^1,2,3,4,5, Yunhua He^1,2,3,4,5,6

¹Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang 524088, China.

Foods (Basel, Switzerland)

|August 14, 2025

概括

在肥胖小鼠中,Hylocereus polyrhizus纸残留物多糖 (HPPP) 通过调节粘液O-糖化,改善了肠道健康. 这项研究揭示了HPPP.

科学领域:

生物化学生物化学
胃肠病学胃肠病学
营养科学营养科学

背景情况:

肥胖和结肠炎通常涉及肠道屏障功能受损.
来自Hylocereus polyrhizus纸残留物 (HPPP) 的多糖体对代谢障碍有希望.
对于HPPP对肠粘液层的精确作用机制,特别是O-糖化,尚不清楚.

研究的目的:

研究HPPP如何影响结肠炎肥胖小鼠结肠粘液层中的O-糖化修饰.
阐明HPPP对饮食引起的肠道损伤的保护机制.

主要方法:

建立高脂肪饮食 (HFD) 诱导的肥胖结肠炎小鼠模型.
使用纳米毛囊液体染色学-并联质谱法 (nanoLC-MS/MS) 进行动态O-糖化变化的定量分析.
对结肠组织的定量O-糖化蛋白质组学和全蛋白质组分析.

主要成果:

在HFD诱导的肥胖大肠炎小鼠的结肠组织中确定了155个特异性改变的O-糖化位点.
观察到MUC2核心蛋白质的糖化修饰水平显著增加 (约2.1倍).
证明HPPP通过调节粘液O-糖化相互作用来减轻结肠粘膜损伤.

结论:

在肥胖小鼠中,HPPP积极调节受高脂肪饮食影响的O-糖化位点.
HPPP治疗改善了肠道粘膜结构,并提供了对肥胖引起的肠道损伤的保护.
这项研究突出了HPPP在调节O-糖化对改善肠道健康的作用.

关键词:

希洛塞鲁斯多利里苏斯 (Hylocereus polyrhizus) 纸残留的多糖化物.代谢综合征是代谢综合征.这是一种O-glycopeptide.抗氧化剂活性抗氧化剂活性特定于特定地点的o-糖蛋白组学.

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