Microbiome of prebiotic-treated mice reveals novel targets involved in host response during obesity.
Microbiome of prebiotic-treated mice reveals novel targets involved in host response during obesity.
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DOI：
10.1038/ismej.2014.45
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发表时间：
2014-10
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--
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中科院分区：
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--
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肠道微生物群参与与肥胖和2型糖尿病相关的代谢和免疫紊乱。我们先前证明，益生元治疗可以通过调节与改善肠道内分泌、屏障和免疫功能相关的细菌种类来显著改善宿主健康。需要对肠道宏基因组进行分析，以确定哪些细菌功能和分类群负责营养干预后有益的微生物-宿主相互作用。我们在生理（对照饮食：CT）和病理条件（高脂饮食：HFD）下对小鼠进行益生元（Pre）处理8周，并研究了肠道抗菌肽和肠道微生物组的产生。HFD喂养显著降低了空肠中再生胰岛衍生的3-γ（Reg 3g）和磷脂酶A2组-II（PLA 2g 2）的表达。益生元治疗增加了Reg 3g的表达（增加了50倍），并改善了肠道的稳态，这是由intectin表达的增加所表明的，intectin是一种参与肠上皮细胞更新的关键蛋白。深度宏基因组测序分析显示，HFD和益生元治疗在不同分类水平上显著影响肠道微生物组。基于蛋白质的邻位组（COG）簇的出现的功能分析还揭示了HFD、Pre、HFD-Pre和CT组的不同特征。最后，益生元诱导的肠道微生物群调节抵消了HFD诱导的炎症和相关代谢紊乱。因此，我们确定了新的推定分类群和代谢功能，可能有助于发展或保护对HFD喂养和HFD-Pre喂养期间观察到的代谢改变。
The gut microbiota is involved in metabolic and immune disorders associated with obesity and type 2 diabetes. We previously demonstrated that prebiotic treatment may significantly improve host health by modulating bacterial species related to the improvement of gut endocrine, barrier and immune functions. An analysis of the gut metagenome is needed to determine which bacterial functions and taxa are responsible for beneficial microbiota–host interactions upon nutritional intervention. We subjected mice to prebiotic (Pre) treatment under physiological (control diet: CT) and pathological conditions (high-fat diet: HFD) for 8 weeks and investigated the production of intestinal antimicrobial peptides and the gut microbiome. HFD feeding significantly decreased the expression of regenerating islet-derived 3-gamma (Reg3g) and phospholipase A2 group-II (PLA2g2) in the jejunum. Prebiotic treatment increased Reg3g expression (by ∼50-fold) and improved intestinal homeostasis as suggested by the increase in the expression of intectin, a key protein involved in intestinal epithelial cell turnover. Deep metagenomic sequencing analysis revealed that HFD and prebiotic treatment significantly affected the gut microbiome at different taxonomic levels. Functional analyses based on the occurrence of clusters of orthologous groups (COGs) of proteins also revealed distinct profiles for the HFD, Pre, HFD-Pre and CT groups. Finally, the gut microbiota modulations induced by prebiotics counteracted HFD-induced inflammation and related metabolic disorders. Thus, we identified novel putative taxa and metabolic functions that may contribute to the development of or protection against the metabolic alterations observed during HFD feeding and HFD-Pre feeding.
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