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Article: Assessment of Causal Direction Between Gut Microbiota-Dependent Metabolites and Cardiometabolic Health: A Bidirectional Mendelian Randomization Analysis

TitleAssessment of Causal Direction Between Gut Microbiota-Dependent Metabolites and Cardiometabolic Health: A Bidirectional Mendelian Randomization Analysis
Authors
Issue Date2019
PublisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/
Citation
Diabetes, 2019, v. 68 n. 9, p. 1747-1755 How to Cite?
AbstractWe examined the causal direction between gut microbiota-dependent metabolite trimethylamine-N-oxide (TMAO) or its predecessors and cardiometabolic diseases such as risk of type 2 diabetes mellitus (T2DM), coronary artery disease (CAD), myocardial infarction (MI), stroke, atrial fibrillation (AF), and chronic kidney disease (CKD). We used genetic variants as instruments to test the causal associations. Genetically predicted higher TMAO and carnitine were not associated with higher odds of T2DM, AF, CAD, MI, stroke, and CKD after Bonferroni correction (P≤0.0005). However, we observed that genetically increased choline showed a suggestive association with higher risk of T2DM (odds ratio: 1.84, 95% confidence interval: 1.00 to 3.42 per 10 units, P=0.05). In contrast, genetically predicted higher betaine (0.68, 0.48 to 0.95 per 10 units, P=0.023) was suggestively associated with a lower risk of T2DM. We observed a suggestive association of genetically increased choline with a lower level of body fat % (beta: -0.28, SE: 0.11, P=0.013), but a higher level of estimated glomerular filtration rate (0.10±0.05, P=0.034). We further found that T2DM (beta: 0.130, SE: 0. 0.036, P<0.0001) and CKD (0.483±0.168, P=0.004) were causally associated with higher TMAO levels. Our MR findings support that T2DM and kidney disease increase TMAO levels and observational evidence for cardiovascular diseases may be due to confounding or reverse causality.
Persistent Identifierhttp://hdl.handle.net/10722/272965
ISSN
2019 Impact Factor: 7.72
2015 SCImago Journal Rankings: 5.185

 

DC FieldValueLanguage
dc.contributor.authorJia, J-
dc.contributor.authorDou, P-
dc.contributor.authorGao, M-
dc.contributor.authorKong, X-
dc.contributor.authorLi, C-
dc.contributor.authorLiu, Z-
dc.contributor.authorHuang, T-
dc.date.accessioned2019-08-06T09:20:01Z-
dc.date.available2019-08-06T09:20:01Z-
dc.date.issued2019-
dc.identifier.citationDiabetes, 2019, v. 68 n. 9, p. 1747-1755-
dc.identifier.issn0012-1797-
dc.identifier.urihttp://hdl.handle.net/10722/272965-
dc.description.abstractWe examined the causal direction between gut microbiota-dependent metabolite trimethylamine-N-oxide (TMAO) or its predecessors and cardiometabolic diseases such as risk of type 2 diabetes mellitus (T2DM), coronary artery disease (CAD), myocardial infarction (MI), stroke, atrial fibrillation (AF), and chronic kidney disease (CKD). We used genetic variants as instruments to test the causal associations. Genetically predicted higher TMAO and carnitine were not associated with higher odds of T2DM, AF, CAD, MI, stroke, and CKD after Bonferroni correction (P≤0.0005). However, we observed that genetically increased choline showed a suggestive association with higher risk of T2DM (odds ratio: 1.84, 95% confidence interval: 1.00 to 3.42 per 10 units, P=0.05). In contrast, genetically predicted higher betaine (0.68, 0.48 to 0.95 per 10 units, P=0.023) was suggestively associated with a lower risk of T2DM. We observed a suggestive association of genetically increased choline with a lower level of body fat % (beta: -0.28, SE: 0.11, P=0.013), but a higher level of estimated glomerular filtration rate (0.10±0.05, P=0.034). We further found that T2DM (beta: 0.130, SE: 0. 0.036, P<0.0001) and CKD (0.483±0.168, P=0.004) were causally associated with higher TMAO levels. Our MR findings support that T2DM and kidney disease increase TMAO levels and observational evidence for cardiovascular diseases may be due to confounding or reverse causality.-
dc.languageeng-
dc.publisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/-
dc.relation.ispartofDiabetes-
dc.rightsThis is an author-created, uncopyedited electronic version of an article accepted for publication in TITLE [Journal URL]. The American Diabetes Association (ADA), publisher of TITLE, is not responsible for any errors or omissions in this version of the manuscript or any version derived from it by third parties. The definitive publisher-authenticated version is available online at [URL]-
dc.titleAssessment of Causal Direction Between Gut Microbiota-Dependent Metabolites and Cardiometabolic Health: A Bidirectional Mendelian Randomization Analysis-
dc.typeArticle-
dc.identifier.emailLiu, Z: zhhliu@hku.hk-
dc.identifier.authorityLiu, Z=rp02429-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2337/db19-0153-
dc.identifier.scopuseid_2-s2.0-85071426193-
dc.identifier.hkuros299713-
dc.identifier.volume68-
dc.identifier.issue9-
dc.identifier.spage1747-
dc.identifier.epage1755-
dc.publisher.placeUnited States-

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