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FRT10干预的高脂饮食诱导肥胖小鼠肝脏和盲肠内容物的代谢组学特征

Metabolomic Characteristics of Liver and Cecum Contents in High-Fat-Diet-Induced Obese Mice Intervened with FRT10.

作者信息

Cai Hongying, Li Daojie, Song Liye, Xu Xin, Han Yunsheng, Meng Kun, Wen Zhiguo, Yang Peilong

机构信息

Key Laboratory of Feed Biotechnology of Ministry of Agriculture and Rural Affairs, Institute of Feed Research, Chinese Academy of Agricultural Sciences, Beijing 100081, China.

National Engineering Research Center of Biological Feed, Beijing 100081, China.

出版信息

Foods. 2022 Aug 18;11(16):2491. doi: 10.3390/foods11162491.

DOI:10.3390/foods11162491
PMID:36010491
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9407591/
Abstract

Obesity has become a major social problem related to health and quality of life. Our previous work demonstrated that FRT10 alleviated obesity in high-fat diet (HFD)-fed mice by alleviating gut dysbiosis. However, the underlying functions of FRT10 in regulating liver and cecum contents metabolism remain unknown. Liver and cecum contents metabonomics combined with pathway analysis based on ultraperformance liquid chromatography-quadrupole-time-of-flight mass spectrometry (UHPLC-Q-TOF/MS) were performed to evaluate the alterations of metabolic profiles between obese control mice and obese mice in FRT10-treated groups. The orthogonal partial least squares discriminant analysis (OPLS-DA) score plots showed that there were significant differences in cecum contents and liver markers between experimental groups. In total, 26 potential biomarkers were identified in the liver and 15 in cecum contents that could explain the effect of FRT10 addition in HFD-fed mice. In addition, gut-liver axis analysis indicated that there was a strong correlation between cecum contents metabolites and hepatic metabolites. The mechanism of FRT10 against obesity might be related to the alterations in glycerophospholipid metabolism, primary bile acid biosynthesis, amino metabolism, and purine and pyrimidine metabolism. Studies on these metabolites could help us better understand the role of FRT10 in obesity induced by HFD.

摘要

肥胖已成为一个与健康和生活质量相关的主要社会问题。我们之前的研究表明,FRT10通过缓解肠道菌群失调减轻了高脂饮食(HFD)喂养小鼠的肥胖。然而,FRT10在调节肝脏和盲肠内容物代谢方面的潜在功能仍不清楚。采用基于超高效液相色谱-四极杆-飞行时间质谱(UHPLC-Q-TOF/MS)的肝脏和盲肠内容物代谢组学结合通路分析,以评估肥胖对照小鼠和FRT10处理组肥胖小鼠之间代谢谱的变化。正交偏最小二乘法判别分析(OPLS-DA)得分图显示,实验组之间盲肠内容物和肝脏标志物存在显著差异。总共在肝脏中鉴定出26种潜在生物标志物,在盲肠内容物中鉴定出15种,这些生物标志物可以解释在HFD喂养小鼠中添加FRT10的效果。此外,肠-肝轴分析表明,盲肠内容物代谢物与肝脏代谢物之间存在很强的相关性。FRT10抗肥胖的机制可能与甘油磷脂代谢、初级胆汁酸生物合成、氨基酸代谢以及嘌呤和嘧啶代谢的改变有关。对这些代谢物的研究有助于我们更好地理解FRT10在HFD诱导的肥胖中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be32/9407591/093ab56aeb6e/foods-11-02491-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be32/9407591/b3c436a194ad/foods-11-02491-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be32/9407591/ddaeda90d205/foods-11-02491-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be32/9407591/093ab56aeb6e/foods-11-02491-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be32/9407591/b3c436a194ad/foods-11-02491-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be32/9407591/ddaeda90d205/foods-11-02491-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be32/9407591/093ab56aeb6e/foods-11-02491-g003.jpg

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