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肠道微生物组和血浆胆汁酸分析可对患者进行分层,以进行抗糖尿病治疗。

Analyses of gut microbiota and plasma bile acids enable stratification of patients for antidiabetic treatment.

机构信息

Shanghai National Research Centre for Endocrine and Metabolic Diseases, State Key Laboratory of Medical Genomics, Shanghai Institute for Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 200025, Shanghai, China.

BGI-Shenzhen, China National GeneBank-Shenzhen, 518083, Shenzhen, China.

出版信息

Nat Commun. 2017 Nov 27;8(1):1785. doi: 10.1038/s41467-017-01682-2.

Abstract

Antidiabetic medication may modulate the gut microbiota and thereby alter plasma and faecal bile acid (BA) composition, which may improve metabolic health. Here we show that treatment with Acarbose, but not Glipizide, increases the ratio between primary BAs and secondary BAs and plasma levels of unconjugated BAs in treatment-naive type 2 diabetes (T2D) patients, which may beneficially affect metabolism. Acarbose increases the relative abundances of Lactobacillus and Bifidobacterium in the gut microbiota and depletes Bacteroides, thereby changing the relative abundance of microbial genes involved in BA metabolism. Treatment outcomes of Acarbose are dependent on gut microbiota compositions prior to treatment. Compared to patients with a gut microbiota dominated by Prevotella, those with a high abundance of Bacteroides exhibit more changes in plasma BAs and greater improvement in metabolic parameters after Acarbose treatment. Our work highlights the potential for stratification of T2D patients based on their gut microbiota prior to treatment.

摘要

抗糖尿病药物可能调节肠道微生物群,从而改变血浆和粪便胆汁酸(BA)组成,这可能改善代谢健康。在这里,我们表明,阿卡波糖治疗而非格列吡嗪治疗可增加未经治疗的 2 型糖尿病(T2D)患者初级 BA 与次级 BA 的比例以及血浆中未结合 BA 的水平,这可能有益于代谢。阿卡波糖增加了肠道微生物群中乳杆菌和双歧杆菌的相对丰度,并消耗了拟杆菌,从而改变了参与 BA 代谢的微生物基因的相对丰度。阿卡波糖的治疗效果取决于治疗前的肠道微生物群组成。与肠道微生物群以普雷沃氏菌为主的患者相比,丰度较高的拟杆菌患者在阿卡波糖治疗后血浆 BA 变化更大,代谢参数改善更明显。我们的工作强调了在治疗前基于患者的肠道微生物群对 T2D 患者进行分层的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cc/5702614/fdb48ecfd443/41467_2017_1682_Fig1_HTML.jpg

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