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十二指肠微生物群的宏基因组学研究揭示了与肥胖的关联。

A Metagenomic Investigation of the Duodenal Microbiota Reveals Links with Obesity.

作者信息

Angelakis Emmanouil, Armougom Fabrice, Carrière Frédéric, Bachar Dipankar, Laugier René, Lagier Jean-Christophe, Robert Catherine, Michelle Caroline, Henrissat Bernard, Raoult Didier

机构信息

URMITE CNRS-IRD 198 UMR 6236, Aix Marseille Université, Faculté de Médecine, 27 Bd Jean Moulin, 13385, Marseille, France.

CNRS, Aix Marseille Université, UMR7282 Enzymology at Interfaces and Physiology of Lipolysis, 13009, Marseille, France.

出版信息

PLoS One. 2015 Sep 10;10(9):e0137784. doi: 10.1371/journal.pone.0137784. eCollection 2015.

Abstract

BACKGROUND

Few studies have tested the small intestine microbiota in humans, where most nutrient digestion and absorption occur. Here, our objective was to examine the duodenal microbiota between obese and normal volunteers using metagenomic techniques.

METHODOLOGY/PRINCIPAL FINDINGS: We tested duodenal samples from five obese and five normal volunteers using 16S rDNA V6 pyrosequencing and Illumina MiSeq deep sequencing. The predominant phyla of the duodenal microbiota were Firmicutes and Actinobacteria, whereas Bacteroidetes were absent. Obese individuals had a significant increase in anaerobic genera (p < 0.001) and a higher abundance of genes encoding Acyl-CoA dehydrogenase (p = 0.0018) compared to the control group. Obese individuals also had a reduced abundance of genes encoding sucrose phosphorylase (p = 0.015) and 1,4-alpha-glucan branching enzyme (p = 0.05). Normal weight people had significantly increased FabK (p = 0.027), and the glycerophospholipid metabolism pathway revealed the presence of phospholipase A1 only in the control group (p = 0.05).

CONCLUSIONS/SIGNIFICANCE: The duodenal microbiota of obese individuals exhibit alterations in the fatty acid and sucrose breakdown pathways, probably induced by diet imbalance.

摘要

背景

很少有研究检测过人类小肠微生物群,而大多数营养物质的消化和吸收都发生在小肠。在此,我们的目标是使用宏基因组技术检查肥胖志愿者和正常志愿者之间的十二指肠微生物群。

方法/主要发现:我们使用16S rDNA V6焦磷酸测序和Illumina MiSeq深度测序检测了五名肥胖志愿者和五名正常志愿者的十二指肠样本。十二指肠微生物群的主要门类是厚壁菌门和放线菌门,而拟杆菌门不存在。与对照组相比,肥胖个体的厌氧属显著增加(p < 0.001),编码酰基辅酶A脱氢酶的基因丰度更高(p = 0.0018)。肥胖个体中编码蔗糖磷酸化酶(p = 0.015)和1,4-α-葡聚糖分支酶(p = 0.05)的基因丰度也降低。正常体重者的FabK显著增加(p = 0.027),甘油磷脂代谢途径显示仅在对照组中存在磷脂酶A1(p = 0.05)。

结论/意义:肥胖个体的十二指肠微生物群在脂肪酸和蔗糖分解途径中表现出改变,可能是由饮食不均衡引起的。

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