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肠道微生物组可能导致肥胖啮齿动物的胰岛素抵抗和全身炎症:一项荟萃分析。

Gut microbiome may contribute to insulin resistance and systemic inflammation in obese rodents: a meta-analysis.

机构信息

Department of Gastroenterology, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University , Shanghai , People's Republic of China.

Digestive Diseases and Nutrition Center, Department of Pediatrics, The State University of New York at Buffalo , Buffalo, New York.

出版信息

Physiol Genomics. 2018 Apr 1;50(4):244-254. doi: 10.1152/physiolgenomics.00114.2017. Epub 2018 Jan 26.


DOI:10.1152/physiolgenomics.00114.2017
PMID:29373083
Abstract

A number of studies have associated obesity with altered gut microbiota, although results are discordant regarding compositional changes in the gut microbiota of obese animals. Herein we used a meta-analysis to obtain an unbiased evaluation of structural and functional changes of the gut microbiota in diet-induced obese rodents. The raw sequencing data of nine studies generated from high-fat diet (HFD)-induced obese rodent models were processed with QIIME to obtain gut microbiota compositions. Biological functions were predicted and annotated with KEGG pathways with PICRUSt. No significant difference was observed for alpha diversity and Bacteroidetes-to-Firmicutes ratio between obese and lean rodents. Bacteroidia, Clostridia, Bacilli, and Erysipelotrichi were dominant classes, but gut microbiota compositions varied among studies. Meta-analysis of the nine microbiome data sets identified 15 differential taxa and 57 differential pathways between obese and lean rodents. In obese rodents, increased abundance was observed for Dorea, Oscillospira, and Ruminococcus, known for fermenting polysaccharide into short chain fatty acids (SCFAs). Decreased Turicibacter and increased Lactococcus are consistent with elevated inflammation in the obese status. Differential functional pathways of the gut microbiome in obese rodents included enriched pyruvate metabolism, butanoate metabolism, propanoate metabolism, pentose phosphate pathway, fatty acid biosynthesis, and glycerolipid metabolism pathways. These pathways converge in the function of carbohydrate metabolism, SCFA metabolism, and biosynthesis of lipid. HFD-induced obesity results in structural and functional dysbiosis of gut microbiota. The altered gut microbiome may contribute to obesity development by promoting insulin resistance and systemic inflammation.

摘要

许多研究都将肥胖与肠道微生物群的改变联系起来,尽管关于肥胖动物肠道微生物群组成的变化,结果并不一致。在此,我们使用荟萃分析来对饮食诱导肥胖啮齿动物的肠道微生物群的结构和功能变化进行无偏评估。对来自高脂肪饮食(HFD)诱导肥胖啮齿动物模型的九项研究的原始测序数据进行了处理,使用 QIIME 获得了肠道微生物群组成。使用 PICRUSt 对生物功能进行了预测和注释,KEGG 途径。肥胖和瘦鼠之间的 alpha 多样性和拟杆菌与厚壁菌比值没有差异。拟杆菌门、梭菌门、芽孢杆菌门和真杆菌门是优势纲,但各研究之间的肠道微生物群组成存在差异。对九组微生物组数据的荟萃分析确定了肥胖和瘦鼠之间 15 个差异分类群和 57 个差异途径。在肥胖啮齿动物中,Dorea、Oscillospira 和 Ruminococcus 的丰度增加,这些菌以发酵多糖产生短链脂肪酸(SCFAs)而闻名。Turicibacter 的减少和 Lactococcus 的增加与肥胖状态下炎症的升高一致。肥胖啮齿动物肠道微生物群的差异功能途径包括丙酮酸代谢、丁酸盐代谢、丙酸盐代谢、戊糖磷酸途径、脂肪酸生物合成和甘油磷脂代谢途径。这些途径集中在碳水化合物代谢、SCFA 代谢和脂质生物合成的功能上。HFD 诱导的肥胖导致肠道微生物群的结构和功能失调。改变的肠道微生物群可能通过促进胰岛素抵抗和全身炎症导致肥胖的发展。

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