期刊
NATURE GENETICS
卷 51, 期 4, 页码 600-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41588-019-0350-x
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资金
- BBMRI-NL
- IN-CONTROL CVON grant [CVON2012-03]
- Top Institute Food and Nutrition (TiFN, Wageningen, the Netherlands) grant [TiFN GH001]
- Netherlands Organization for Scientific Research (NWO) [NWO-VENI 016.176.006, NWO-VIDI 864.13.013, NWO-VIDI 016.Vidi.178.056]
- NWO Spinoza Prizes [SPI 92-266, SPI 94-212]
- European Research Council (ERC) [715772]
- FP7/2007-2013/ERC Advanced Grant [2012-322698]
- ERC [310372]
- Tripartite Immunometabolism consortium (TrIC)-Novo Nordisk Foundation grant [NNF15CC0018486]
- Wellcome grants [090532, 098381, 106130, 203141]
- Rosalind Franklin Fellowship from the University of Groningen
- TarGet
Microbiome-wide association studies on large population cohorts have highlighted associations between the gut microbiome and complex traits, including type 2 diabetes (T2D) and obesity(1). However, the causal relationships remain largely unresolved. We leveraged information from 952 normoglycemic individuals for whom genome-wide genotyping, gut metagenomic sequence and fecal short-chain fatty acid (SCFA) levels were available(2), then combined this information with genome-wide-association summary statistics for 17 metabolic and anthropometric traits. Using bidirectional Mendelian randomization (MR) analyses to assess causality(3), we found that the host-genetic-driven increase in gut production of the SCFA butyrate was associated with improved insulin response after an oral glucose-tolerance test (P = 9.8 x 10(-5)), whereas abnormalities in the production or absorption of another SCFA, propionate, were causally related to an increased risk of T2D (P = 0.004). These data provide evidence of a causal effect of the gut microbiome on metabolic traits and support the use of MR as a means to elucidate causal relationships from microbiome-wide association findings.
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