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灰树花多糖的结构表征及其对高脂饮食喂养小鼠胰岛素抵抗的影响。

Structure characterization of Grifola frondosa polysaccharide and its effect on insulin resistance in HFD-fed mice.

作者信息

Ding Yin-Yi, Lan Jinchi, Wang Yuxin, Pan Yuxiang, Song Tianyuan, Liu Shizhu, Gu Zhenyu, Ge Yujun

机构信息

National Experimental Teaching Demonstration Center of Food Engineering and Quality and Safety, Food (Edible Fungi) Processing Technology Research Center, School of Food Science and Biotechnology, Zhejiang Gongshang University, Hangzhou, 310018, China.

Zhejiang Fangge Pharmaceutical Co. Ltd, Lishui, 323800, China.

出版信息

NPJ Sci Food. 2025 Jan 8;9(1):3. doi: 10.1038/s41538-024-00359-7.

DOI:10.1038/s41538-024-00359-7
PMID:39774946
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11707143/
Abstract

Polysaccharide extracted from Grifola frondosa (GFP) was selected in this study. After preliminary separation, four factions were collected, named GFP-F1, GFP-F2, GFP-F3 and GFP-F4. GPF-F2 was further separated into two fractions, namely GFP-N1 and GFP-N2. The molecular weight of GFP-N1 and GFP-N2 was 3.323×10kDa and 10.8 kDa, respectively. GFP-N1 was composed of glucose and galactose and 1 → 3, 1 → 4, and 1 → 6 glycosidic bonds. GFP-N2 was composed of glucose, galactose and mannose and 1 → 2, 1 → 3, 1 → 4, and 1 → 6 glycosidic bonds. GFP could significantly relieve the insulin resistance induced by HFD. GFP significantly alleviated gut microbiota disturbance caused by HFD and increased the production of short-chain fatty acids, and further reduced the expression of LPS/TLR4 inflammatory pathway. GFP significantly reduced the oxidative stress induced by HFD, increased the expression of the Nrf2/ARE signaling pathway. These results indicated that GFP could be developed as a potential ingredient for the management of insulin resistance.

摘要

本研究选用了从云芝中提取的多糖(GFP)。经过初步分离,收集到四个组分,分别命名为GFP-F1、GFP-F2、GFP-F3和GFP-F4。GFP-F2进一步分离为两个组分,即GFP-N1和GFP-N2。GFP-N1和GFP-N2的分子量分别为3.323×10 kDa和10.8 kDa。GFP-N1由葡萄糖和半乳糖以及1→3、1→4和1→6糖苷键组成。GFP-N2由葡萄糖、半乳糖和甘露糖以及1→2、1→3、1→4和1→6糖苷键组成。GFP可显著缓解高脂饮食诱导的胰岛素抵抗。GFP显著减轻了高脂饮食引起的肠道微生物群紊乱,增加了短链脂肪酸的产生,并进一步降低了LPS/TLR4炎症通路的表达。GFP显著降低了高脂饮食诱导的氧化应激,增加了Nrf2/ARE信号通路的表达。这些结果表明,GFP可开发成为一种用于管理胰岛素抵抗的潜在成分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/11707143/9fff3e35b9f0/41538_2024_359_Fig10_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/11707143/9fff3e35b9f0/41538_2024_359_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/11707143/cabcbb1030ae/41538_2024_359_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/11707143/c387a1c735af/41538_2024_359_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/11707143/03423e404c3a/41538_2024_359_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/11707143/e7958e35c0cf/41538_2024_359_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/11707143/0b38c44234d2/41538_2024_359_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d3c/11707143/9fff3e35b9f0/41538_2024_359_Fig10_HTML.jpg

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