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首页> 外文期刊>EBioMedicine >Dietary Modulation of Gut Microbiota Contributes to Alleviation of Both Genetic and Simple Obesity in Children
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Dietary Modulation of Gut Microbiota Contributes to Alleviation of Both Genetic and Simple Obesity in Children

机译：肠道菌群的饮食调节有助于缓解儿童遗传性肥胖和单纯性肥胖

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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.
机译：肠道菌群被认为是饮食相关肥胖的关键因素。然而，它在人类遗传性肥胖症（如普拉德-威利综合症（PWS））疾病表型发展中的作用仍然难以捉摸。在这项针对PWS（n = 17）和单纯性肥胖（n = 21）儿童的住院干预试验中，富含非消化性碳水化合物的饮食会导致体重显着减轻和肠道菌群的结构变化，并降低血清抗原负荷和减轻炎症。直接从宏基因组学数据集中组装的161个流行细菌吃水基因组的共丰网络分析表明，碳水化合物发酵产生乙酸盐的功能基因组相对增加。基于NMR的尿代谢组谱分析显示饮食引起的宿主代谢型总体变化，并鉴定出三甲基胺N-氧化物和吲哚酚硫酸盐显着降低，这是宿主细菌的协同代谢产物，可引起代谢恶化。发现与这些有害的共代谢物的尿液水平相关的特定细菌基因组编码了通过肠道中胆碱或色氨酸发酵产生其前体的酶基因。当将其移植到无菌小鼠中时，与来自同一志愿者的干预后微生物菌群相比，干预前的肠道菌群诱导了更高的炎症和更大的脂肪细胞。我们基于多组学的系统分析表明，不良生物肠道菌群对儿童遗传性肥胖和单纯性肥胖都有重要的病因学贡献，暗示了潜在的有效缓解目标。背景研究：饮食管理不善和基因突变是肥胖相关疾病毁灭性流行背后的两个主要驱动力。缺乏对驱动力和疾病终点之间因果关系的分子链的了解，阻碍了疾病预防和治疗的进展。我们发现，患有Prader-Willi综合征的遗传性肥胖儿童与饮食相关性肥胖的儿童相比，其肠道菌群具有类似的营养不良。富含不可消化但可发酵的碳水化合物的饮食显着促进了有益细菌群的产生，并减少了毒素的产生，无论主要的驱动力如何，都有助于减轻肥胖者的代谢恶化。

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