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Dietary modulation of gut microbiota contributes to alleviation of both genetic and simple obesity in children.

Zhang, Chenhong and Yin, Aihua and Li, Hongde and Wang, Ruirui and Wu, Guojun and Shen, Jian and Menghui, Zhang and Wang, Linghua and Hou, Yaping and Ouyang, Haimei and Zhang, Yan and Zheng, Yinan and Wang, Jicheng and Lv, Xiaofei and Wang, Yulan and Zhang, Feng and Zeng, Benhua and Li, Wenxia and Yan, Feiyan and Zhao, Yufeng and Pang, Xiaoyan and Zhang, Xiaojun and Fu, Huaqing and Chen, Feng and Zhao, Naisi and Hamaker, Bruce R. and Bridgewater, Laura C. and Weinkove, David and Clement, Karine and Dore, Joel and Holmes, Elaine and Xiao, Huasheng and Zhao, Guoping and Yang, Shengli and Bork, Peer and Nicholson, Jeremy K. and Wei, Hong and Tang, Huiru and Zhang, Xiaozhuang and Zhao, Liping (2015) 'Dietary modulation of gut microbiota contributes to alleviation of both genetic and simple obesity in children.', EBioMedicine., 2 (8). pp. 968-984.


Gut microbiota has been implicated as a pivotal contributing factor in diet-related obesity; however, its role in development of disease phenotypes in human genetic obesity such as Prader–Willi syndrome (PWS) remains elusive. In this hospitalized intervention trial with PWS (n = 17) and simple obesity (n = 21) children, a diet rich in non-digestible carbohydrates induced significant weight loss and concomitant structural changes of the gut microbiota together with reduction of serum antigen load and alleviation of inflammation. Co-abundance network analysis of 161 prevalent bacterial draft genomes assembled directly from metagenomic datasets showed relative increase of functional genome groups for acetate production from carbohydrates fermentation. NMR-based metabolomic profiling of urine showed diet-induced overall changes of host metabotypes and identified significantly reduced trimethylamine N-oxide and indoxyl sulfate, host-bacteria co-metabolites known to induce metabolic deteriorations. Specific bacterial genomes that were correlated with urine levels of these detrimental co-metabolites were found to encode enzyme genes for production of their precursors by fermentation of choline or tryptophan in the gut. When transplanted into germ-free mice, the pre-intervention gut microbiota induced higher inflammation and larger adipocytes compared with the post-intervention microbiota from the same volunteer. Our multi-omics-based systems analysis indicates a significant etiological contribution of dysbiotic gut microbiota to both genetic and simple obesity in children, implicating a potentially effective target for alleviation.

Item Type:Article
Keywords:Prader–Willi syndrome, Obesity, Gut microbiota, Metagenomics, Metabolomics, Genome interaction network
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Available under License - Creative Commons Attribution Non-commercial No Derivatives.
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Publisher statement:© 2015 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (
Date accepted:11 September 2015
Date deposited:29 October 2015
Date of first online publication:August 2015
Date first made open access:No date available

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