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牙髓残渣多糖通过调节肠道黏液分泌和糖基化减轻高脂饮食诱导的肥胖。

Pulp Residues Polysaccharide Alleviates High-Fat Diet-Induced Obesity by Modulating Intestinal Mucus Secretion and Glycosylation.

作者信息

Li Guanghui, Cheong Kit-Leong, He Yunhua, Liew Ahluk, Huang Jiaxuan, Huang Chen, Zhong Saiyi, Sathuvan Malairaj

机构信息

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.

出版信息

Foods. 2025 Aug 1;14(15):2708. doi: 10.3390/foods14152708.


DOI:10.3390/foods14152708
PMID:40807645
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12345779/
Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/8b2a44d3243c/foods-14-02708-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/4721e0cf5a3d/foods-14-02708-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/23cbe0e671e7/foods-14-02708-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/46011f963e5f/foods-14-02708-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/858cb4625454/foods-14-02708-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/0c8525a86230/foods-14-02708-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/8b2a44d3243c/foods-14-02708-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/4721e0cf5a3d/foods-14-02708-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/23cbe0e671e7/foods-14-02708-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/46011f963e5f/foods-14-02708-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/858cb4625454/foods-14-02708-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/0c8525a86230/foods-14-02708-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eafe/12345779/8b2a44d3243c/foods-14-02708-g006.jpg

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本文引用的文献

[1]
Structure-function relationship of the brown seaweed Undaria pinnatifida laminaran: Protein kinase C-mediated mucus secretion and gut barrier restoration.

Carbohydr Polym. 2025-6-15

[2]
The role of bariatric surgery in hypertension control: a systematic review and meta-analysis with extended benefits on metabolic factors.

BMC Cardiovasc Disord. 2025-3-24

[3]
Dietary polysaccharides from dragon fruit pomace, a co-product of the fruit processing industry, exhibit therapeutic potential in high-fat diet-induced metabolic disorders.

Food Res Int. 2025-2

[4]
Seed Oil Reduces the Severity of Colitis Induced by Dextran Sulfate Sodium by Modulating the Intestinal Microbiota and Restoring the Intestinal Barrier.

Foods. 2024-8-24

[5]
Antibiotics damage the colonic mucus barrier in a microbiota-independent manner.

Sci Adv. 2024-9-13

[6]
Dual Regulation Mechanism of Obesity: DNA Methylation and Intestinal Flora.

Biomedicines. 2024-7-23

[7]
In vivo mapping of the mouse Galnt3-specific O-glycoproteome.

J Biol Chem. 2024-9

[8]
O-glycosylation of SARS-CoV-2 spike protein by host O-glycosyltransferase strengthens its trimeric structure.

Acta Biochim Biophys Sin (Shanghai). 2024-7-26

[9]
B3galt5 functions as a PXR target gene and regulates obesity and insulin resistance by maintaining intestinal integrity.

Nat Commun. 2024-7-14

[10]
Global incidence, prevalence, years lived with disability (YLDs), disability-adjusted life-years (DALYs), and healthy life expectancy (HALE) for 371 diseases and injuries in 204 countries and territories and 811 subnational locations, 1990-2021: a systematic analysis for the Global Burden of Disease Study 2021.

Lancet. 2024-5-18

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