Gut microbiome-related effects of berberine and probiotics on type 2 diabetes (the PREMOTE study)
Human gut microbiome is a promising target for managing type 2 diabetes (T2D). Measures altering gut microbiota like oral intake of probiotics or berberine (BBR), a bacteriostatic agent, merit metabolic homoeostasis. We hence conducted a randomized, double-blind, placebo-controlled trial with newly...
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| Published in | Nature communications Vol. 11; no. 1; pp. 5015 - 12 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
06.10.2020
Nature Portfolio |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2041-1723 2041-1723 |
| DOI | 10.1038/s41467-020-18414-8 |
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| Abstract | Human gut microbiome is a promising target for managing type 2 diabetes (T2D). Measures altering gut microbiota like oral intake of probiotics or berberine (BBR), a bacteriostatic agent, merit metabolic homoeostasis. We hence conducted a randomized, double-blind, placebo-controlled trial with newly diagnosed T2D patients from 20 centres in China. Four-hundred-nine eligible participants were enroled, randomly assigned (1:1:1:1) and completed a 12-week treatment of either BBR-alone, probiotics+BBR, probiotics-alone, or placebo, after a one-week run-in of gentamycin pretreatment. The changes in glycated haemoglobin, as the primary outcome, in the probiotics+BBR (least-squares mean [95% CI], −1.04[−1.19, −0.89]%) and BBR-alone group (−0.99[−1.16, −0.83]%) were significantly greater than that in the placebo and probiotics-alone groups (−0.59[−0.75, −0.44]%, −0.53[−0.68, −0.37]%, P < 0.001). BBR treatment induced more gastrointestinal side effects. Further metagenomics and metabolomic studies found that the hypoglycaemic effect of BBR is mediated by the inhibition of DCA biotransformation by
Ruminococcus bromii
. Therefore, our study reports a human microbial related mechanism underlying the antidiabetic effect of BBR on T2D. (Clinicaltrial.gov Identifier: NCT02861261).
The gut microbiome affects systemic metabolism and is a therapeutic target for type 2 diabetes. Here the authors demonstrate in a randomized controlled trial that effects of berberine, a plant alkaloid known to lower blood glucose, may be explained by the inhibition of
Ruminococcus bromii
mediated biotransformation of the bile acid deoxycholic acid. |
|---|---|
| AbstractList | Human gut microbiome is a promising target for managing type 2 diabetes (T2D). Measures altering gut microbiota like oral intake of probiotics or berberine (BBR), a bacteriostatic agent, merit metabolic homoeostasis. We hence conducted a randomized, double-blind, placebo-controlled trial with newly diagnosed T2D patients from 20 centres in China. Four-hundred-nine eligible participants were enroled, randomly assigned (1:1:1:1) and completed a 12-week treatment of either BBR-alone, probiotics+BBR, probiotics-alone, or placebo, after a one-week run-in of gentamycin pretreatment. The changes in glycated haemoglobin, as the primary outcome, in the probiotics+BBR (least-squares mean [95% CI], −1.04[−1.19, −0.89]%) and BBR-alone group (−0.99[−1.16, −0.83]%) were significantly greater than that in the placebo and probiotics-alone groups (−0.59[−0.75, −0.44]%, −0.53[−0.68, −0.37]%, P < 0.001). BBR treatment induced more gastrointestinal side effects. Further metagenomics and metabolomic studies found that the hypoglycaemic effect of BBR is mediated by the inhibition of DCA biotransformation by
Ruminococcus bromii
. Therefore, our study reports a human microbial related mechanism underlying the antidiabetic effect of BBR on T2D. (Clinicaltrial.gov Identifier: NCT02861261). Human gut microbiome is a promising target for managing type 2 diabetes (T2D). Measures altering gut microbiota like oral intake of probiotics or berberine (BBR), a bacteriostatic agent, merit metabolic homoeostasis. We hence conducted a randomized, double-blind, placebo-controlled trial with newly diagnosed T2D patients from 20 centres in China. Four-hundred-nine eligible participants were enroled, randomly assigned (1:1:1:1) and completed a 12-week treatment of either BBR-alone, probiotics+BBR, probiotics-alone, or placebo, after a one-week run-in of gentamycin pretreatment. The changes in glycated haemoglobin, as the primary outcome, in the probiotics+BBR (least-squares mean [95% CI], -1.04[-1.19, -0.89]%) and BBR-alone group (-0.99[-1.16, -0.83]%) were significantly greater than that in the placebo and probiotics-alone groups (-0.59[-0.75, -0.44]%, -0.53[-0.68, -0.37]%, P < 0.001). BBR treatment induced more gastrointestinal side effects. Further metagenomics and metabolomic studies found that the hypoglycaemic effect of BBR is mediated by the inhibition of DCA biotransformation by Ruminococcus bromii. Therefore, our study reports a human microbial related mechanism underlying the antidiabetic effect of BBR on T2D. (Clinicaltrial.gov Identifier: NCT02861261).Human gut microbiome is a promising target for managing type 2 diabetes (T2D). Measures altering gut microbiota like oral intake of probiotics or berberine (BBR), a bacteriostatic agent, merit metabolic homoeostasis. We hence conducted a randomized, double-blind, placebo-controlled trial with newly diagnosed T2D patients from 20 centres in China. Four-hundred-nine eligible participants were enroled, randomly assigned (1:1:1:1) and completed a 12-week treatment of either BBR-alone, probiotics+BBR, probiotics-alone, or placebo, after a one-week run-in of gentamycin pretreatment. The changes in glycated haemoglobin, as the primary outcome, in the probiotics+BBR (least-squares mean [95% CI], -1.04[-1.19, -0.89]%) and BBR-alone group (-0.99[-1.16, -0.83]%) were significantly greater than that in the placebo and probiotics-alone groups (-0.59[-0.75, -0.44]%, -0.53[-0.68, -0.37]%, P < 0.001). BBR treatment induced more gastrointestinal side effects. Further metagenomics and metabolomic studies found that the hypoglycaemic effect of BBR is mediated by the inhibition of DCA biotransformation by Ruminococcus bromii. Therefore, our study reports a human microbial related mechanism underlying the antidiabetic effect of BBR on T2D. (Clinicaltrial.gov Identifier: NCT02861261). Human gut microbiome is a promising target for managing type 2 diabetes (T2D). Measures altering gut microbiota like oral intake of probiotics or berberine (BBR), a bacteriostatic agent, merit metabolic homoeostasis. We hence conducted a randomized, double-blind, placebo-controlled trial with newly diagnosed T2D patients from 20 centres in China. Four-hundred-nine eligible participants were enroled, randomly assigned (1:1:1:1) and completed a 12-week treatment of either BBR-alone, probiotics+BBR, probiotics-alone, or placebo, after a one-week run-in of gentamycin pretreatment. The changes in glycated haemoglobin, as the primary outcome, in the probiotics+BBR (least-squares mean [95% CI], −1.04[−1.19, −0.89]%) and BBR-alone group (−0.99[−1.16, −0.83]%) were significantly greater than that in the placebo and probiotics-alone groups (−0.59[−0.75, −0.44]%, −0.53[−0.68, −0.37]%, P < 0.001). BBR treatment induced more gastrointestinal side effects. Further metagenomics and metabolomic studies found that the hypoglycaemic effect of BBR is mediated by the inhibition of DCA biotransformation by Ruminococcus bromii . Therefore, our study reports a human microbial related mechanism underlying the antidiabetic effect of BBR on T2D. (Clinicaltrial.gov Identifier: NCT02861261). The gut microbiome affects systemic metabolism and is a therapeutic target for type 2 diabetes. Here the authors demonstrate in a randomized controlled trial that effects of berberine, a plant alkaloid known to lower blood glucose, may be explained by the inhibition of Ruminococcus bromii mediated biotransformation of the bile acid deoxycholic acid. The gut microbiome affects systemic metabolism and is a therapeutic target for type 2 diabetes. Here the authors demonstrate in a randomized controlled trial that effects of berberine, a plant alkaloid known to lower blood glucose, may be explained by the inhibition of Ruminococcus bromii mediated biotransformation of the bile acid deoxycholic acid. |
| ArticleNumber | 5015 |
| Author | Zou, Yuanqiang Gu, Yanyun Li, Qi Lai, Shenghan Li, Junhua Chen, Li Peng, Yongde Ren, Huahui Huang, Shan Kong, Ping Wang, Shujie Chen, Gang Wang, Xiaolin Qiu, Yixuan Xue, Yaoming Hou, Guixue Li, Xuelin Yang, Huanming Xu, Guowang Ning, Guang Qu, Shen Wang, Jian Zhao, Xinjie Zhong, Huanzi Gao, Mengyu Zhang, Yifei Gu, Xuejiang Liang, Jun Qin, Li Wang, Weiqing Ma, Jing Shi, Zhun Huang, Qin Yang, Jialin |
| Author_xml | – sequence: 1 givenname: Yifei orcidid: 0000-0003-0272-0602 surname: Zhang fullname: Zhang, Yifei organization: National Clinical Research Centre for Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 2 givenname: Yanyun surname: Gu fullname: Gu, Yanyun organization: National Clinical Research Centre for Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 3 givenname: Huahui surname: Ren fullname: Ren, Huahui organization: BGI-Shenzhen – sequence: 4 givenname: Shujie orcidid: 0000-0001-8838-4771 surname: Wang fullname: Wang, Shujie organization: National Clinical Research Centre for Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 5 givenname: Huanzi orcidid: 0000-0001-9512-1750 surname: Zhong fullname: Zhong, Huanzi organization: BGI-Shenzhen – sequence: 6 givenname: Xinjie surname: Zhao fullname: Zhao, Xinjie organization: Dalian Institute of Chemical Physics, Chinese Academy of Science – sequence: 7 givenname: Jing surname: Ma fullname: Ma, Jing organization: Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 8 givenname: Xuejiang surname: Gu fullname: Gu, Xuejiang organization: The First Affiliated hospital of Wenzhou Medical University – sequence: 9 givenname: Yaoming surname: Xue fullname: Xue, Yaoming organization: Nanfang Hospital, Southern Medical University – sequence: 10 givenname: Shan surname: Huang fullname: Huang, Shan organization: Tong Ren Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 11 givenname: Jialin surname: Yang fullname: Yang, Jialin organization: Central Hospital of Minhang District – sequence: 12 givenname: Li surname: Chen fullname: Chen, Li organization: Qilu Hospital of Shandong University – sequence: 13 givenname: Gang surname: Chen fullname: Chen, Gang organization: Fujian Provincial Hospital – sequence: 14 givenname: Shen surname: Qu fullname: Qu, Shen organization: Shanghai Tenth People’s Hospital of Tong Ji University – sequence: 15 givenname: Jun surname: Liang fullname: Liang, Jun organization: Xuzhou Central Hospital – sequence: 16 givenname: Li surname: Qin fullname: Qin, Li organization: Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 17 givenname: Qin surname: Huang fullname: Huang, Qin organization: Chang Hai Hospital, Second Military Medical University – sequence: 18 givenname: Yongde surname: Peng fullname: Peng, Yongde organization: Shanghai First People’s Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 19 givenname: Qi surname: Li fullname: Li, Qi organization: Dalian Institute of Chemical Physics, Chinese Academy of Science – sequence: 20 givenname: Xiaolin surname: Wang fullname: Wang, Xiaolin organization: Dalian Institute of Chemical Physics, Chinese Academy of Science – sequence: 21 givenname: Ping surname: Kong fullname: Kong, Ping organization: BGI-Shenzhen – sequence: 22 givenname: Guixue orcidid: 0000-0003-0342-9593 surname: Hou fullname: Hou, Guixue organization: BGI-Shenzhen – sequence: 23 givenname: Mengyu surname: Gao fullname: Gao, Mengyu organization: BGI-Shenzhen – sequence: 24 givenname: Zhun surname: Shi fullname: Shi, Zhun organization: BGI-Shenzhen – sequence: 25 givenname: Xuelin surname: Li fullname: Li, Xuelin organization: National Clinical Research Centre for Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 26 givenname: Yixuan surname: Qiu fullname: Qiu, Yixuan organization: National Clinical Research Centre for Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 27 givenname: Yuanqiang surname: Zou fullname: Zou, Yuanqiang organization: BGI-Shenzhen – sequence: 28 givenname: Huanming surname: Yang fullname: Yang, Huanming organization: BGI-Shenzhen, James D. Watson Institute of Genome Sciences – sequence: 29 givenname: Jian surname: Wang fullname: Wang, Jian organization: BGI-Shenzhen, James D. Watson Institute of Genome Sciences – sequence: 30 givenname: Guowang surname: Xu fullname: Xu, Guowang organization: Dalian Institute of Chemical Physics, Chinese Academy of Science – sequence: 31 givenname: Shenghan surname: Lai fullname: Lai, Shenghan organization: Johns Hopkins University School of Medicine – sequence: 32 givenname: Junhua orcidid: 0000-0001-6784-1873 surname: Li fullname: Li, Junhua email: lijunhua@genomics.cn organization: BGI-Shenzhen, School of Biology and Biological Engineering, South China University of Technology – sequence: 33 givenname: Guang surname: Ning fullname: Ning, Guang organization: National Clinical Research Centre for Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 34 givenname: Weiqing surname: Wang fullname: Wang, Weiqing email: wqingw61@163.com organization: National Clinical Research Centre for Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine |
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| Snippet | Human gut microbiome is a promising target for managing type 2 diabetes (T2D). Measures altering gut microbiota like oral intake of probiotics or berberine... The gut microbiome affects systemic metabolism and is a therapeutic target for type 2 diabetes. Here the authors demonstrate in a randomized controlled trial... |
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| Title | Gut microbiome-related effects of berberine and probiotics on type 2 diabetes (the PREMOTE study) |
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