赵立平团队:先天肥胖?不怕,用饮食纠正!

富含不易消化糖类的饮食导致体重明显减轻、肠道菌群变化及炎症的缓解。
161种肠道菌群宏基因组分析发现产乙酸相关基因的增加。
尿液的代谢组分析表明氧化三甲胺和硫酸吲哚酚的合成显著降低。这些肠道菌群代谢物会增加炎症风险。
多组学系统分析表明了肠道菌群与遗传性及单纯性肥胖的密切关系。
延伸阅读
EBioMedicine [IF:6.183]

Dietary Modulation of Gut Microbiota Contributes to Alleviation of Both Genetic and Simple Obesity in Children

通过饮食调节肠道菌群可缓解儿童遗传性及单纯性肥胖

2015-07-10, Article, 10.1016/j.ebiom.2015.07.007more

Abstract:
UNLABELLED: 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.
RESEARCH IN CONTEXT: Poorly managed diet and genetic mutations are the two primary driving forces behind the devastating epidemic of obesity-related diseases. Lack of understanding of the molecular chain of causation between the driving forces and the disease endpoints retards progress in prevention and treatment of the diseases. We found that children genetically obese with Prader-Willi syndrome shared a similar dysbiosis in their gut microbiota with those having diet-related obesity. A diet rich in non-digestible but fermentable carbohydrates significantly promoted beneficial groups of bacteria and reduced toxin-producers, which contributes to the alleviation of metabolic deteriorations in obesity regardless of the primary driving forces.

First Authors:
Chenhong Zhang,Aihua Yin,Hongde Li,Ruirui Wang,Guojun Wu,Jian Shen

Correspondence Authors:
Huiru Tang,Xiaozhuang Zhang,Liping Zhao

All Authors:
Chenhong Zhang,Aihua Yin,Hongde Li,Ruirui Wang,Guojun Wu,Jian Shen,Menghui Zhang,Linghua Wang,Yaping Hou,Haimei Ouyang,Yan Zhang,Yinan Zheng,Jicheng Wang,Xiaofei Lv,Yulan Wang,Feng Zhang,Benhua Zeng,Wenxia Li,Feiyan Yan,Yufeng Zhao,Xiaoyan Pang,Xiaojun Zhang,Huaqing Fu,Feng Chen,Naisi Zhao,Bruce R Hamaker,Laura C Bridgewater,David Weinkove,Karine Clement,Joel Dore,Elaine Holmes,Huasheng Xiao,Guoping Zhao,Shengli Yang,Peer Bork,Jeremy K Nicholson,Hong Wei,Huiru Tang,Xiaozhuang Zhang,Liping Zhao