A metabolomics study: Could plasma metabolites be a guide for the prevention of tamsulosin side effects?

Akman, Tuğrul Çağrı; Kadıoğlu, Yücel; Şenol, Onur; Erkayman, Beyzagül

doi:10.1016/j.pharma.2022.09.004

Cited by 1 publication

(1 citation statement)

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“…Previous researchers tend to conduct metabolomics studies to prevent asthenia caused by the side effects of drugs. For example, some authors screened the signi cantly related metabolite to suggest vitamin A and D supplements prevent the asthenia induced by tamsulosin 12 . According to the fact that metabolism is one of the underlying factors associated with asthenia, Metabolomics analysis is a possible breach for preventing and healing asthenia.…”

Section: Introductionmentioning

confidence: 99%

Causality of genetically determined metabolites and metabolic pathways on asthenia: a two-sample Mendelian randomization study

Jing,

Jia,

et al. 2024

Preprint

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Objectives Previous studies attempted to relieve drug-related asthenia by analyzing the blood metabolites. Metabolism as a potential mechanism of asthenia may be a clue for developing effective prevention and treatment methods. This study aimed to explore the causal relationship of metabolites or metabolic pathways to asthenia. Methods We adopted single nucleotide polymorphisms (SNPs) as genetic instruments to evaluate the levels of 486 circulating metabolites. These SNPs were obtained from large-scale genome-wide association studies originating from Europe. We investigated the causal impact of genetically predicted circulating metabolites on asthenia by a two-sample Mendelian randomization (MR) analysis. The sensitivity analysis estimated the reliability of the results, containing MR-Egger, weighted median, and weighted mode. Every one standard deviation (SD) elevation in exposure was revealed as odds ratios (OR) with 95% confidence intervals (CIs). Results After screening 486 circulating metabolites in this MR, we identified a causal relationship between 17 metabolites and asthenia. Among which bilirubin Z (IVW OR = 0.956; 95% CI: 0.934–0.979; P < 0.01), myristoleate (OR = 0.903; 95% CI: 0.822–0.993; P = 0.035), N-acetylalanine (OR = 0.961; 95% CI: 0.938–0.985; P = 0.001), threonate (OR = 0.922; 95% CI: 0.857–0.991; P = 0.028), 1-methylxanthine (OR = 0.917; 95% CI: 0.859–0.978; P = 0.009) were causally associated with reduced risk of asthenia. Arachidonate (OR = 1.305; 95% CI: 1.165–1.462; P < 0.01), kynurenine (OR = 1.204; 95% CI: 1.067–1.359; P = 0.003), lysine (OR = 1.335; 95% CI: 1.116–1.597; P = 0.002), octadecanedioate (OR = 1.121; 95% CI: 1.041–1.208; P = 0.003), oleoylcarnitine (OR = 1.161; 95% CI: 1.015–1.329; P = 0.030), palmitoleate (OR = 1.231; 95% CI: 1.023–1.480; P = 0.028), stearoylcarnitine (OR = 1.194; 95% CI: 1.042–1.369; P = 0.011), thymol sulfate (OR = 1.035; 95% CI: 1.011–1.059; P = 0.004), valine (OR = 2.042; 95% CI: 1.400-2.979; P < 0.01), 3-dehydrocarnitine (OR = 1.182; 95% CI: 1.076-1.300; P < 0.01), 4-methyl-2-oxopentanoate (OR = 1.235; 95% CI: 1.009–1.511; P = 0.040), 4-vinylphenol sulfate (OR = 1.098; 95% CI: 1.046–1.153; P < 0.01) were related to a higher risk of asthenia. This result is not affected by heterogeneity and horizontal pleiotropy. Metabolic pathway analysis suggested three pathways that probably correlated to asthenia, they were “Glycine, serine and threonine metabolism (P = 0.00174)”, “Glycerophospholipid metabolism (P = 0.0304)”, “Phenylalanine, tyrosine and tryptophan biosynthesis (P = 0.0309)”. Conclusions This MR study discovered a causal effect of blood metabolites on the asthenia risk. These metabolites and metabolic pathways can be applied in asthenia prevention and treatment strategies.

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Section: Introductionmentioning

confidence: 99%