Author
Listed:
- Yanyun Gu
(Shanghai Jiaotong University School of Medicine)
- Xiaokai Wang
(China National GeneBank-Shenzhen
University of Chinese Academy of Sciences)
- Junhua Li
(China National GeneBank-Shenzhen
BGI-Shenzhen)
- Yifei Zhang
(Shanghai Jiaotong University School of Medicine)
- Huanzi Zhong
(China National GeneBank-Shenzhen
University of Copenhagen)
- Ruixin Liu
(Shanghai Jiaotong University School of Medicine)
- Dongya Zhang
(China National GeneBank-Shenzhen)
- Qiang Feng
(China National GeneBank-Shenzhen)
- Xiaoyan Xie
(Shanghai Jiaotong University School of Medicine)
- Jie Hong
(Shanghai Jiaotong University School of Medicine)
- Huahui Ren
(China National GeneBank-Shenzhen
BGI-Shenzhen
BGI-Shenzhen)
- Wei Liu
(Renji Hospital affiliated to Shanghai Jiaotong University Medical School)
- Jing Ma
(Renji Hospital affiliated to Shanghai Jiaotong University Medical School)
- Qing Su
(Xinhua Hospital affiliated to Shanghai Jiaotong University Medical School)
- Hongmei Zhang
(Xinhua Hospital affiliated to Shanghai Jiaotong University Medical School)
- Jialin Yang
(MinHang Central Hospital affiliated to Fudan University Medical School)
- Xiaoling Wang
(Chinese Academy of Science)
- Xinjie Zhao
(Chinese Academy of Science)
- Weiqiong Gu
(Shanghai Jiaotong University School of Medicine)
- Yufang Bi
(Shanghai Jiaotong University School of Medicine)
- Yongde Peng
(Shanghai Jiaotong University)
- Xiaoqiang Xu
(China National GeneBank-Shenzhen
University of Chinese Academy of Sciences)
- Huihua Xia
(China National GeneBank-Shenzhen
BGI-Shenzhen)
- Fang Li
(China National GeneBank-Shenzhen
BGI-Shenzhen
BGI-Shenzhen)
- Xun Xu
(China National GeneBank-Shenzhen)
- Huanming Yang
(China National GeneBank-Shenzhen
James D. Watson Institute of Genome Sciences)
- Guowang Xu
(Chinese Academy of Science)
- Lise Madsen
(China National GeneBank-Shenzhen
University of Chinese Academy of Sciences
National Institute of Nutrition and Seafood Research (NIFES))
- Karsten Kristiansen
(China National GeneBank-Shenzhen
University of Copenhagen)
- Guang Ning
(Shanghai Jiaotong University School of Medicine)
- Weiqing Wang
(Shanghai Jiaotong University School of Medicine)
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.
Suggested Citation
Yanyun Gu & Xiaokai Wang & Junhua Li & Yifei Zhang & Huanzi Zhong & Ruixin Liu & Dongya Zhang & Qiang Feng & Xiaoyan Xie & Jie Hong & Huahui Ren & Wei Liu & Jing Ma & Qing Su & Hongmei Zhang & Jialin , 2017.
"Analyses of gut microbiota and plasma bile acids enable stratification of patients for antidiabetic treatment,"
Nature Communications, Nature, vol. 8(1), pages 1-12, December.
Handle:
RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01682-2
DOI: 10.1038/s41467-017-01682-2
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