Human blood metabolites and risk of sepsis: A Mendelian randomization investigation

孟德尔随机化 败血症 医学 优势比 全基因组关联研究 内科学 置信区间 肿瘤科 遗传学 生物 单核苷酸多态性 基因型 遗传变异 基因
作者
Weifeng Shang,Hang Qian,Sheng Zhang,Mingyang Yuan,Xiaojun Pan,Sisi Huang,Jiao Liu,Dechang Chen
出处
期刊:European Journal of Clinical Investigation [Wiley]
卷期号:54 (4) 被引量:11
标识
DOI:10.1111/eci.14145
摘要

Abstract Background Evidence supports the observational correlations between human blood metabolites and sepsis. However, whether these associations represent a causal relationship is unknown. In this study, we applied two‐sample Mendelian randomization (MR) analyses to examine causality between genetically proxied 486 blood metabolites and sepsis risk. Methods We used summary data from genome‐wide association studies (GWAS) on 486 metabolites involving 7824 individuals as exposure and a sepsis GWAS including 11,643 cases and 474,841 controls as the outcome. The inverse‐variance weighted (IVW) was the primary method to estimate the causal relationship between exposure and outcome, with MR‐Egger and weighted median serving as supplements. Sensitivity analyses were implemented with Cochrane's Q test, MR‐Egger intercept, MR‐PRESSO and leave‐one‐out analysis. In addition, we performed replication MR, meta‐analysis, Steiger test, linkage disequilibrium score (LDSC) regression and multivariable MR (MVMR) to thoroughly verify the causation. Results We identified that genetically determined high levels of 1‐oleoylglycerophosphoethanolamine (odds ratio (OR) = .52, 95% confidence interval (CI): .31–.87, p = .0122), alpha‐glutamyltyrosine (OR = .75, 95% CI: .60–.93, p = .0102), heptanoate (7:0) (OR = .51, 95% CI: .33–.81, p = .0041) and saccharin (OR = .84, 95% CI: .74–.94, p = .0036) were causally associated with a lower risk of sepsis. MVMR analysis demonstrated the independent causal effect of these metabolites on sepsis. Conclusions These findings indicated that four blood metabolites have a protective impact on sepsis, thus providing novel perspectives into the metabolite‐mediated development mechanism of sepsis by combining genomics and metabolomics.
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