Metabolomic signatures for liver tissue and cecum contents in high-fat diet-induced obese mice based on UHPLC-Q-TOF/MS.
Metabolomic signatures for liver tissue and cecum contents in high-fat diet-induced obese mice based on UHPLC-Q-TOF/MS.
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基于 UHPLC-Q-TOF/MS 的高脂饮食诱导肥胖小鼠肝组织和盲肠内容物的代谢组学特征
DOI：
10.1186/s12986-021-00595-8
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发表时间：
2021-06-30
影响因子：
4.5
通讯作者：
Yang P
中科院分区：
文献类型：
--
作者：
Cai H;Wen Z;Meng K;Yang P
肥胖症的发病率在全球范围内不断增加，它是糖尿病、血脂异常和非酒精性脂肪肝的危险因素。我们先前的研究表明，高脂饮食诱导小鼠体重增加，脂肪重量，血清胆固醇，甘油三酯和肝脏中ATL水平增加，并影响盲肠微生物群的多样性和组成。因此，本研究旨在研究肠道微生物衍生代谢物和肝脏代谢物在肥胖和瘦小鼠之间的作用，重点是它们与高脂饮食（HFD）诱导的肥胖进展的关系。用高脂饮食16周建立小鼠肥胖模型。采用超高效液相色谱-四极杆-飞行时间质谱联用技术和正交偏最小二乘判别分析（OPLS-DA）技术对肥胖小鼠盲肠内容物和肝脏组织代谢物进行了研究。OPLS-DA评分图上肥胖组和瘦组明显区分开来，导致区分的主要代谢产物主要涉及甘油磷脂代谢、初级胆汁酸生物合成和不饱和脂肪酸生物合成途径。HFD诱导的肝脏中19种代谢物和盲肠内容物中43种代谢物的变化被确定为与肥胖相关的潜在生物标志物。具体而言，肝中的鹅去氧胆酸、牛磺鹅去氧胆酸盐和牛磺熊去氧胆酸分别升高35.94、24.36和18.71倍。盲肠中的PI（P-16：0/18：1（9 Z））、PG（19：0/16：0）、PS（P-16：0/20：2（11 Z，14 Z））、PI（22：1（11 Z）/12：0）和PE（21：0/0：0）比瘦小鼠增加了884、640.96、226.63、210.10、45.13倍。这些代谢物是区分肥胖和瘦小鼠的最重要的生物标志物。此外，肠-肝轴分析表明盲肠内容物代谢产物与肝脏代谢产物具有较强的相关性。HFD增加肝脏和盲肠中的脂质谱（即甘油磷脂、PC、PE、PI、PG和PS）和总胆汁酸（初级和次级胆汁酸），表明它们可能在肥胖的进展中起重要作用。这些代谢产物可用于更好地了解HFD诱导的肥胖和相关疾病。此外，这些代谢物的水平变化可用于评估肥胖的风险和肥胖管理的治疗效果。
The incidence of obesity is increasing worldwide, and it is a risk factor for diabetes, dyslipidemia, and nonalcoholic fatty liver disease. Our previous study had demonstrated that high-fat diet induced increased weight gain, fat weight, serum cholesterol, triglyceride, and ATL levels in liver, and influenced the diversity and composition of cecal microbiota in mice. Hence, this study aimed to investigate the roles of the gut microbially derived metabolites and liver metabolites between the obese and lean mice, focusing on their association with the progression of obesity induced by high-fat diet (HFD). An obesity model in mice was established with HFD for 16 weeks. Cecal contents and liver tissues metabolomics based on ultraperformance liquid chromatography-quadrupole-time-of-flight mass spectrometry and orthogonal partial least squares discriminant analyses (OPLS-DA) was performed to identify the alterations in metabolites associated with obese mice. Obese and lean groups were clearly discriminated from each other on OPLS-DA score plot and major metabolites contributing to the discrimination were mainly involved in glycerophospholipid metabolism, primary bile acid biosynthesis, and biosynthesis of unsaturated fatty acids pathways. HFD-induced alterations of 19 metabolites in liver and 43 metabolites in cecum contents were identified as potential biomarkers related to obesity. Specifically, chenodeoxycholic acid, taurochenodeoxycholate, and tauroursodeoxycholic acid in liver were elevated 35.94, 24.36, and 18.71-fold, respectively. PI(P-16:0/18:1(9Z)), PG(19:0/16:0), PS(P-16:0/20:2(11Z,14Z)), PI(22:1(11Z)/12:0), and PE(21:0/0:0) in cecum were enhanced 884, 640.96, 226.63, 210.10, 45.13-fold in comparison with the lean mice. These metabolites were the most important biomarkers for discriminating between the obese and lean mice. In addition, cecum contents metabolites were strongly correlated with hepatic metabolites through gut-liver axis analysis. HFD increased lipid profiles (i.e. glycerophospholipids, PC, PE, PI, PG, and PS) and total bile acid (primary and secondary bile acid) in liver and cecum, suggesting that they may play an important role in the progression of obesity. These metabolites can be used to better understand obesity and related disease induced by HFD. Furthermore, the level alterations of these metabolites can be used to assess the risk of obesity and the therapeutic effect of obesity management.
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DOI：
10.1002/oby.21855
发表时间：
2017-06
期刊：
Obesity (Silver Spring, Md.)
影响因子：
--
作者：
Han J;Dzierlenga AL;Lu Z;Billheimer DD;Torabzadeh E;Lake AD;Li H;Novak P;Shipkova P;Aranibar N;Robertson D;Reily MD;Lehman-McKeeman LD;Cherrington NJ
通讯作者：
Cherrington NJ
植物乳杆菌 FRT10 通过调节 PPAR α 信号通路和肠道微生物群缓解高脂饮食诱导的小鼠肥胖
影响因子：
5
作者：
Cai, Hongying;Wen, Zhiguo;Yang, Peilong
通讯作者：
Yang, Peilong
影响因子：
2.6
作者：
Ma, Ning;Liu, Xi-Wang;Li, Jian-Yong
通讯作者：
Li, Jian-Yong
生命早期补充叶绿素可预防饮食引起的肥胖并调节小鼠肠道微生物群
影响因子：
5.2
作者：
Li, Yuanyuan;Cui, Yu;Zhang, Yan
通讯作者：
Zhang, Yan
影响因子：
2.1
作者：
Marshall, JC
通讯作者：
Marshall, JC