Journal
NATURE MEDICINE
Volume 23, Issue 7, Pages 850-+Publisher
NATURE RESEARCH
DOI: 10.1038/nm.4345
Keywords
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Funding
- Swedish Diabetes Foundation
- Swedish Research Council
- Swedish Heart Lung Foundation
- Torsten Soderberg's Foundation
- Goran Gustafsson's Foundation
- Inga Britt and Arne Lundberg's Foundation
- Swedish Foundation for Strategic Research
- Knut and Alice Wallenberg Foundation
- Novo Nordisk Foundation
- Region Vastra Gotaland
- Sahlgrenska University Hospital
- Ministerio de Economia y Competitividad [PI11-00214, PI15/01934]
- FEDER funds
- Obra Social Fundacion la Caixa fellowship under the Severo Ochoa program
- Sara Borrell Fellowship from the Instituto Carlos III
- EFSD/Lilly Research Fellowship
- Beatriu de Pinos Fellowship from the Agency for Management of University and Research Grants (AGAUR)
- ERC Consolidator Grant (European Research Council) [615362-METABASE]
- NNF Center for Basic Metabolic Research [Bäckhed Group] Funding Source: researchfish
- Novo Nordisk Fonden [NNF13OC0008163, NNF15OC0016798] Funding Source: researchfish
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Metformin is widely used in the treatment of type 2 diabetes (T2D), but its mechanism of action is poorly defined. Recent evidence implicates the gut microbiota as a site of metformin action. In a double-blind study, we randomized individuals with treatment-naive T2D to placebo or metformin for 4 months and showed that metformin had strong effects on the gut microbiome. These results were verified in a subset of the placebo group that switched to metformin 6 months after the start of the trial. Transfer of fecal samples (obtained before and 4 months after treatment) from metformin-treated donors to germ-free mice showed that glucose tolerance was improved in mice that received metformin-altered microbiota. By directly investigating metformin-microbiota interactions in a gut simulator, we showed that metformin affected pathways with common biological functions in species from two different phyla, and many of the metformin-regulated genes in these species encoded metalloproteins or metal transporters. Our findings provide support for the notion that altered gut microbiota mediates some of metformin's antidiabetic effects.
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