Assessment of Causal Direction Between Gut Microbiota-Dependent Metabolites and Cardiometabolic Health: Abi-Directional Mendelian Randomisation Analysis.

Clicks: 443
ID: 4711
2019
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #2 of 50 articles by views in Diabetes

Most read Least read

Bar heights use a square-root scale.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
We 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.
Reference Key
jia2019assessmentdiabetes Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Jia, Jinzhu;Dou, Pan;Gao, Meng;Kong, Xuejun;Li, Changwei;Liu, Zhonghua;Huang, Tao;
Journal Diabetes
Year 2019
DOI
db190153
URL
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.