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

Jialin Yang, Weiqing Wang, Guang Ning, Karsten Kristiansen, Lise Madsen, Guowang Xu, Huanming Yang, Xun Xu, Fang Li, Huihua Xia, Xiaoqiang Xu, Yongde Peng, Yufang Bi, Weiqiong Gu, Xinjie Zhao, Xiaoling Wang, Yanyun Gu, Hongmei Zhang, Qing Su, Jing Ma, Wei Liu, Huahui Ren, Jie Hong, Xiaoyan Xie, Qiang Feng, Dongya Zhang, Ruixin Liu, Huanzi Zhong, Yifei Zhang, Junhua Li, Xiaokai Wang

Journal: Nature communications 2018;8(1):1785

PMID: 29176714

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.

Address: 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.; BGI Education Centre, University of Chinese Academy of Sciences, 518083, Shenzhen, China.; Shenzhen Key Laboratory of Human commensal microorganisms and Health Research, BGI-Shenzhen, Shenzhen, 518083, China.; Laboratory of Genomics and Molecular Biomedicine, Department of Biology, University of Copenhagen, 2100, Copenhagen, Denmark.; Shenzhen Engineering Laboratory of Detection and Intervention of human intestinal microbiome, BGI-Shenzhen, Shenzhen, 518083, China.; Renji Hospital affiliated to Shanghai Jiaotong University Medical School, 200127, Shanghai, China.; Xinhua Hospital affiliated to Shanghai Jiaotong University Medical School, 200092, Shanghai, China.; MinHang Central Hospital affiliated to Fudan University Medical School, 201100, Shanghai, China.; Dalian Institute of Chemical Physics, Chinese Academy of Science, 116011, Dalian, China.; Shanghai General Hospital, Shanghai Jiaotong University, 200080, Shanghai, China.; James D. Watson Institute of Genome Sciences, Hangzhou, 310008, China.; National Institute of Nutrition and Seafood Research (NIFES), 5817, Bergen, Norway.; BGI-Shenzhen, China National GeneBank-Shenzhen, 518083, Shenzhen, China. [email protected].; Laboratory of Genomics and Molecular Biomedicine, Department of Biology, University of Copenhagen, 2100, Copenhagen, Denmark. [email protected].; 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. [email protected].; 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. [email protected].
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