Fecal microbiota and bile acid interactions with systemic and adipose tissue metabolism in diet-induced weight loss of obese postmenopausal women.
Fecal microbiota and bile acid interactions with systemic and adipose tissue metabolism in diet-induced weight loss of obese postmenopausal women.
复制标题
DOI：
10.1186/s12967-018-1619-z
复制
发表时间：
2018-09-03
影响因子：
7.4
通讯作者：
Holt PR
中科院分区：
文献类型：
--
作者：
Alemán JO;Bokulich NA;Swann JR;Walker JM;De Rosa JC;Battaglia T;Costabile A;Pechlivanis A;Liang Y;Breslow JL;Blaser MJ;Holt PR
胃肠道中的微生物群和胆汁酸深刻地改变全身代谢过程。在肥胖受试者中，逐渐减轻体重可改善脂肪组织炎症和相关的全身变化。我们评估了极低热量饮食（VLCD）导致的快速体重减轻如何影响粪便微生物组和粪便胆汁酸组成，以及它们与肥胖症患者血浆代谢组和皮下脂肪组织炎症的相互作用。我们在一个代谢单位的10名2-3级肥胖绝经后妇女中进行了一项VLCD诱导体重减轻10%的前瞻性队列研究。基线和体重减轻后评估包括通过质谱分析的空腹血浆、通过RNA测序分析的脂肪组织转录、粪便微生物群的粪便16 S rRNA测序、通过质谱分析的粪便胆汁酸和通过1H-NMR光谱分析的尿代谢表型。结果指标包括粪便微生物群和胆汁酸组成变化与血浆代谢物和脂肪组织基因表达途径变化之间的混合模型相关性。VLCD诱导的体重减轻后尿代谢表型的改变与饥饿酮症、蛋白质节约和肠道微生物群功能状态的破坏一致。我们发现，在VLCD诱导的体重减轻过程中，核心微生物组被保留下来，但几组细菌分类群发生了变化，具有功能意义。UniFrac分析显示，群落结构总体上平行变化，对应于罗斯拜瑞氏菌属丰度的减少和克里斯滕森菌科丰度的增加;g__（未知属）。估算的微生物功能显示脂肪和碳水化合物代谢的变化。粪便总胆汁酸浓度显著下降，解结合和7-α-二羟基化减少，伴随着几种细菌分类群的显著变化。粪便中的单个胆汁酸与血浆中的氨基酸、嘌呤和脂质代谢途径相关。此外，几种粪便胆汁酸和细菌种类与脂肪组织中改变的基因表达途径相关。肥胖女性的VLCD饮食干预改变了几种粪便微生物群的组成，同时保留了核心粪便微生物组。个体微生物类群及其功能的变化与血浆代谢组、粪便胆汁酸组成和脂肪组织转录组的变化相关。试验注册ClinicalTrials.gov NCT 01699906，2012年10月4日，Retroplasty注册。URL-https：clinicaltrials.gov/ct2/show/NCT01699906本文的在线版本（10.1186/s12967-018-1619-z）包含补充材料，可供授权用户使用。
Microbiota and bile acids in the gastrointestinal tract profoundly alter systemic metabolic processes. In obese subjects, gradual weight loss ameliorates adipose tissue inflammation and related systemic changes. We assessed how rapid weight loss due to a very low calorie diet (VLCD) affects the fecal microbiome and fecal bile acid composition, and their interactions with the plasma metabolome and subcutaneous adipose tissue inflammation in obesity. We performed a prospective cohort study of VLCD-induced weight loss of 10% in ten grades 2–3 obese postmenopausal women in a metabolic unit. Baseline and post weight loss evaluation included fasting plasma analyzed by mass spectrometry, adipose tissue transcription by RNA sequencing, stool 16S rRNA sequencing for fecal microbiota, fecal bile acids by mass spectrometry, and urinary metabolic phenotyping by 1H-NMR spectroscopy. Outcome measures included mixed model correlations between changes in fecal microbiota and bile acid composition with changes in plasma metabolite and adipose tissue gene expression pathways. Alterations in the urinary metabolic phenotype following VLCD-induced weight loss were consistent with starvation ketosis, protein sparing, and disruptions to the functional status of the gut microbiota. We show that the core microbiome was preserved during VLCD-induced weight loss, but with changes in several groups of bacterial taxa with functional implications. UniFrac analysis showed overall parallel shifts in community structure, corresponding to reduced abundance of the genus Roseburia and increased Christensenellaceae;g__ (unknown genus). Imputed microbial functions showed changes in fat and carbohydrate metabolism. A significant fall in fecal total bile acid concentration and reduced deconjugation and 7-α-dihydroxylation were accompanied by significant changes in several bacterial taxa. Individual bile acids in feces correlated with amino acid, purine, and lipid metabolic pathways in plasma. Furthermore, several fecal bile acids and bacterial species correlated with altered gene expression pathways in adipose tissue. VLCD dietary intervention in obese women changed the composition of several fecal microbial populations while preserving the core fecal microbiome. Changes in individual microbial taxa and their functions correlated with variations in the plasma metabolome, fecal bile acid composition, and adipose tissue transcriptome. Trial Registration ClinicalTrials.gov NCT01699906, 4-Oct-2012, Retrospectively registered. URL-https://clinicaltrials.gov/ct2/show/NCT01699906 The online version of this article (10.1186/s12967-018-1619-z) contains supplementary material, which is available to authorized users.
登录
查看更多内容
影响因子：
48
作者：
Callahan BJ;McMurdie PJ;Rosen MJ;Han AW;Johnson AJ;Holmes SP
通讯作者：
Holmes SP
影响因子：
5.9
作者：
FAITH, DP
通讯作者：
FAITH, DP
肠道选择性法尼醇 X 受体抑制可改善肥胖相关的代谢功能障碍。
影响因子：
16.6
作者：
Jiang C;Xie C;Lv Y;Li J;Krausz KW;Shi J;Brocker CN;Desai D;Amin SG;Bisson WH;Liu Y;Gavrilova O;Patterson AD;Gonzalez FJ
通讯作者：
Gonzalez FJ
影响因子：
--
作者：
Damms-Machado A;Mitra S;Schollenberger AE;Kramer KM;Meile T;Königsrainer A;Huson DH;Bischoff SC
通讯作者：
Bischoff SC
影响因子：
4.1
作者：
Alemán JO;Iyengar NM;Walker JM;Milne GL;Da Rosa JC;Liang Y;Giri DD;Zhou XK;Pollak MN;Hudis CA;Breslow JL;Holt PR;Dannenberg AJ
通讯作者：
Dannenberg AJ