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基于超高效液相色谱-四极杆飞行时间质谱联用技术的代谢组学揭示了多糖(HLP)调节糖尿病大鼠血清代谢变化的机制。

UPLC-Q-TOF/MS-based metabonomics reveals mechanisms for polysaccharides (HLP)-regulated serum metabolic changes in diabetic rats.

作者信息

Zhang Xin, Zhao Fuqiang, Ma Tingting, Zheng Yuanping, Cao Jun, Li Chuan, Zhu Kexue

机构信息

Engineering Research Center of Utilization of Tropical Polysaccharide Resources of Ministry of Education, School of Food Science and Engineering, Hainan University, Haikou 570228, China.

Collaborative Innovation Center of Provincial and Ministerial Co-construction for Marine Food Deep Processing, Dalian Polytechnic University, Dalian 116034, China.

出版信息

Food Chem X. 2023 Jun 16;19:100741. doi: 10.1016/j.fochx.2023.100741. eCollection 2023 Oct 30.

DOI:10.1016/j.fochx.2023.100741
PMID:37780338
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10534105/
Abstract

This study aimed to use metabolomic methods to explore how polysaccharides (HLP) improved metabolism disorders in the liver of Goto-Kakizaki (GK) rats with spontaneous type 2 diabetes. The results showed that HLP effectively improved the metabolic disorder. Based on KEGG functional analysis, five key biomarkers associated with bile acid metabolism were detected and screened ( < 0.05). The results of serum total bile acid levels and liver damage in diabetic rats further showed the regulatory effects of HLP on bile acid metabolism. The results of bile acid-related gene expression in the liver showed that HLP inhibited liver farnesoid X Receptor - small heterodimer partner (FXR-SHP) signalling and increased the expression of bile acid synthesis genes ( < 0.05). Our results explored the underlying mechanisms by which HLP accelerated cholesterol consumption to anti-hypercholesterolemia and anti-diabetic by inhibiting liver FXR-SHP signaling. HLP's effect on bile acid regulation provides insights into treating T2DM.

摘要

本研究旨在运用代谢组学方法,探究多糖(HLP)如何改善自发性2型糖尿病的Goto-Kakizaki(GK)大鼠肝脏中的代谢紊乱。结果表明,HLP有效改善了代谢紊乱。基于KEGG功能分析,检测并筛选出与胆汁酸代谢相关的5个关键生物标志物(<0.05)。糖尿病大鼠血清总胆汁酸水平和肝损伤结果进一步显示了HLP对胆汁酸代谢的调节作用。肝脏中胆汁酸相关基因表达结果表明,HLP抑制肝脏法尼醇X受体-小异二聚体伴侣(FXR-SHP)信号传导,并增加胆汁酸合成基因的表达(<0.05)。我们的研究结果探索了HLP通过抑制肝脏FXR-SHP信号传导加速胆固醇消耗以抗高胆固醇血症和抗糖尿病的潜在机制。HLP对胆汁酸的调节作用为治疗2型糖尿病提供了思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341e/10534105/aa6f76e5e8c9/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341e/10534105/c9234cd7a5d2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341e/10534105/d0b0ad0cdbf8/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341e/10534105/ca9b5accfe07/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341e/10534105/aa6f76e5e8c9/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341e/10534105/c9234cd7a5d2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341e/10534105/d0b0ad0cdbf8/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341e/10534105/ca9b5accfe07/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341e/10534105/aa6f76e5e8c9/gr4.jpg

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Foods. 2021 Oct 21;10(11):2528. doi: 10.3390/foods10112528.
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