GC-TOF-MS-Based Metabolomics Analyses of Liver and Intestinal Contents in the Overfed vs. Normally-Fed Geese.
GC-TOF-MS-Based Metabolomics Analyses of Liver and Intestinal Contents in the Overfed vs. Normally-Fed Geese.
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基于 GC-TOF-MS 的代谢组学分析过度喂养与正常喂养鹅的肝脏和肠道内容物
DOI：
10.3390/ani10122375
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发表时间：
2020-12-11
期刊：
影响因子：
--
通讯作者：
Gong D
中科院分区：
文献类型：
--
作者：
Zhao M;Xing Y;Liu L;Fan X;Liu L;Geng T;Gong D
非酒精性脂肪性肝病一直被认为是肝脏疾病的重要原因之一，在全球范围内威胁着人类和动物的健康。有趣的是，鹅脂肪肝可以达到正常肝脏重量的8-10倍，没有明显的病理症状，这表明存在一些保护机制。科学家们指出，肠道微生物区系参与了人类和哺乳动物非酒精性脂肪性肝病的形成。然而，目前还不清楚肠道微生物区系及其代谢产物是否与鹅脂肪肝有关。本研究的目的是对超饲和正常饲喂鹅的肝脏和肠道内容物进行代谢组学分析。结果表明，鹅脂肪肝的形成伴随着肝脏和肠道内容物代谢谱的明显变化。肠道代谢产物可通过影响葡萄糖和脂肪酸的代谢、氧化应激和炎症反应来影响鹅脂肪肝的形成。这些发现为今后解决肠道代谢物与非酒精性脂肪性肝病的发展之间的关系提供了基础。在严重脂肪变性的鹅肝脏中没有观察到明显的病理症状，这表明鹅可能具有独特的保护机制。以气相色谱-飞行时间-质谱仪为基础的代谢组学分析方法，对饲喂过量和正常饲喂的鹅(每组各26只)的肝脏和肠道内容物进行了分析。我们发现，过量喂养显著改变了肝脏和肠道内容物的代谢特征。差异代谢物主要有脂肪酸、氨基酸、有机酸和胺类。这些差异代谢物涉及糖酵解/糖异生、甘油脂代谢、戊糖磷酸途径、脂肪酸降解、鞘磷脂信号通路和不饱和脂肪酸的生物合成。此外，我们还测定了花生四烯酸(ARA)和四氢皮质酮(TD)对鹅原代肝细胞和肠道细胞的生物学效应。结果表明，0.50 mM ARA可显著诱导鹅原代肠道细胞花生四烯酸5-脂氧合酶(ALOX5)基因的表达。1µM TD可显著抑制鹅原代肝细胞细胞色素P-450 27A1(CYP27A1)基因的表达。总之，鹅脂肪肝的形成伴随着肝脏和肠道内容物代谢谱的显著变化，这些变化与葡萄糖和脂肪酸的代谢、氧化应激和炎症反应密切相关。
Non-alcoholic fatty liver disease has been considered as one of the most important causes of liver disease, and it is a threat to human and animal health worldwide. Interestingly, goose fatty liver can reach 8–10 times the weight of normal liver with no overt pathological symptoms, suggesting that there are some protective mechanisms. Scientists have indicated that gut microbiota participate in the formation of non-alcoholic fatty liver disease in human and mammalian animals. However, it is unclear whether gut microbiota and their metabolites contribute to goose fatty liver. The aim of the present study was to investigate the metabolomic analyses of liver and intestinal contents in overfed vs. normally fed geese. The results showed that the formation of goose fatty liver is accompanied by obvious changes in the metabolic profiles of liver and intestinal contents. The intestinal metabolites can affect the formation of goose fatty liver by affecting the metabolisms of glucose and fatty acid, oxidative stress, and inflammatory reactions. These findings provide a basis for future work addressing the relationship between intestinal metabolites and the development of non-alcoholic fatty liver disease. No overt pathological symptoms are observed in the goose liver with severe steatosis, suggesting that geese may host unique protective mechanisms. Gas chromatography time-of-flight mass spectrometry-based metabolomics analyses of liver and intestinal contents in overfed vs. normally fed geese (26 geese in each treatment) were investigated. We found that overfeeding significantly changed the metabolic profiles of liver and intestinal contents. The differential metabolites mainly belong to fatty acids, amino acids, organic acids, and amines. The differential metabolites were involved in glycolysis/gluconeogenesis, glycerolipid metabolism, the pentose phosphate pathway, fatty acid degradation, the sphingolipid signaling pathway, and the biosynthesis of unsaturated fatty acids. Moreover, we determined the biological effects of arachidonic acid (ARA) and tetrahydrocorticosterone (TD) in goose primary hepatocytes and intestinal cells. Data showed that the mRNA expression of arachidonate 5-lipoxygenase (ALOX5) in goose primary intestinal cells was significantly induced by 0.50 mM ARA treatment. Cytochrome P-450 27A1 (CYP27A1) mRNA expression was significantly inhibited in goose primary hepatocytes by 1 µM TD treatment. In conclusion, the formation of goose fatty liver is accompanied by significant changes in the metabolic profiles of liver and intestinal contents, and the changes are closely related to the metabolisms of glucose and fatty acids, oxidative stress, and inflammatory reactions.
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影响因子：
7
作者：
Starick SR;Ibn-Salem J;Jurk M;Hernandez C;Love MI;Chung HR;Vingron M;Thomas-Chollier M;Meijsing SH
通讯作者：
Meijsing SH
独特的脂肪肝模型中的前列腺癌和保护性成分：肠道微生物群和抑制补体系统
影响因子：
4.6
作者：
Liu L;Zhao X;Wang Q;Sun X;Xia L;Wang Q;Yang B;Zhang Y;Montgomery S;Meng H;Geng T;Gong D
通讯作者：
Gong D
影响因子：
25.7
作者：
Allard, Johane P.;Aghdassi, Elaheh;Heathcote, Jenny E.
通讯作者：
Heathcote, Jenny E.
影响因子：
4.1
作者：
VESSEY, DA;WHITNEY, J;GOLLAN, JL
通讯作者：
GOLLAN, JL
DOI：
10.1016/0005-2760(94)90143-0
发表时间：
1994-02-10
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA-LIPIDS AND LIPID METABOLISM
影响因子：
--
作者：
HERMIER, D;ROUSSELOTPAILLEY, D;SELLIER, N
通讯作者：
SELLIER, N