Selenium deficiency-induced multiple tissue damage with dysregulation of immune and redox homeostasis in broiler chicks under heat stress

Venous thromboembolism (VTE), chronic venous disease (CVD), and venous leg ulceration (VLU) are clinical manifestations of a poorly functioning venous system. Though common, much is unknown of the pathophysiology and progression of these conditions. Metabolic phenotyping has been employed to explore mechanistic pathways involved in venous disease. A systematic literature review was performed: full text, primary research articles on the applications of nuclear magnetic resonance spectroscopy (NMR) and mass spectrometry (MS) in human participants and animals were included for qualitative synthesis. Seventeen studies applying metabolic phenotyping to venous disease were identified: six on CVD, two on VLU, and nine on VTE; both animal (n = 6) and human (n = 10) experimental designs were reported, with one study including both. NMR, MS, and MS imaging were employed to characterize serum, plasma, urine, wound fluid, and tissue. Metabolites found to be upregulated in CVD included lipids, branched chain amino acids (BCAA), glutamate, taurine, lactate, and myo-inositol identified in vein tissue. Upregulated metabolites in VLU included lactate, BCAA, lysine, 3-hydroxybutyrate, and glutamate identified in wound fluid and ulcer biopsies. VTE cases were associated with reduced carnitine levels, upregulated aromatic amino acids, 3-hydroxybutyrate, BCAA, and lipids in plasma, serum, thrombus, and vein wall; kynurenine and tricarboxylic acid pathway dysfunction were reported. Future research should focus on targeted studies with internal and external validation.

Metabolic Phenotyping in Venous Disease: The Need for Standardization.

Thrombosis is a relatively common human disease, being the third cause of mortality worldwide. Alterations in hemostasis, endothelial processes and blood flow are the major features involved in the pathophysiology of the disease, whose molecular basis is not yet fully understood due to the complexity and numerous influences that might lead to blood clotting. The activity and the role of blood metabolites in thrombosis are attracting great attention in the quest of understanding the triggering off uncontrolled clotting. Metabolomics can bring insights into metabolic fingerprints of any biological sample, quantify, and measure the metabolic responses to the pathophysiological stimuli or genetic modifications, and lead to an integrated comprehension of metabolites function in health and disease. Furthermore, the identification of biomarkers can reveal metabolic pathways associated with the pathogenesis and progression of the disease. In this review, we summarized the current state of knowledge of metabolomics in arterial and venous thrombosis research by nuclear magnetic resonance spectroscopy and mass spectrometry approaches and cited and discussed the altered metabolites that have been cited in both conditions. It is worth stating that the contribution of the metabolomics in this field or research is modest and being introduced in some case studies, and expected to grow in the near future.

Thrombosis: Current knowledge based on metabolomics by nuclear magnetic resonance (NMR) spectroscopy and mass spectrometry (MS)

Plasma and urine metabonomics coupled with UPLC-Q-TOF/MS and multivariate data analysis on potential biomarkers in anemia and hematinic effects of steamed notoginseng

Deep vein thrombosis (DVT) refers to the abnormal coagulation of blood in a deep vein. Recently, some studies have found that metabolites are related to the occurrence of DVT and may serve as new markers for the diagnosis of DVT. In this study, we used the GWAS summary dataset of blood metabolites and DVT to perform a large-scale genetic correlation scan of DVT and blood metabolites to explore the correlation between blood metabolites and DVT. We used GWAS summary data of DVT from the UK Biobank (UK Biobank fields: 20002) and GWAS summary data of blood metabolites from a previously published study (including 529 metabolites in plasma or serum from 7824 adults from two European population studies) for genetic correlation analysis. Then, we conducted a causal study between the screened blood metabolites and DVT by Mendelian randomization (MR) analysis. In the first stage, genetic correlation analysis identified 9 blood metabolites that demonstrated a suggestive association with DVT. These metabolites included Valine (correlation coefficient = 0.2440, P value = 0.0430), Carnitine (correlation coefficient = 0.1574, P value = 0.0146), Hydroxytryptophan (correlation coefficient = 0.2376, P value = 0.0360), and 1-stearoylglycerophosphoethanolamine (correlation coefficient = - 0.3850, P value = 0.0258). Then, based on the IVW MR model, we analysed the causal relationship between the screened blood metabolites and DVT and found that there was a suggestive causal relationship between Hydroxytryptophan (exposure) and DVT (outcome) (β = - 0.0378, se = 0.0163, P = 0.0204). Our study identified a set of candidate blood metabolites that showed a suggestive association with DVT. We hope that our findings will provide new insights into the pathogenesis and diagnosis of DVT in the future. 

/pdf/large-scale-genetic-correlation-scanning-and-causal-1nw6dxy3.pdf

Large-scale genetic correlation scanning and causal association between deep vein thrombosis and human blood metabolites

Deep vein thrombosis (DVT) and pulmonary embolism (PE) have high morbidity, reduce quality of life, and can cause death. Biomarkers or genetic risk factors have not been identified in patients with DVT. In present study, serum of 61 patients suffering from DVT and a rat DVT model (n = 10) were assayed by a proton nuclear magnetic resonance (1H NMR) metabolomics technique combing with multivariate statistical analysis to identify the metabolites. The MetPA platform was used to identify differences in the metabolic pathways between the rat model and patients. The metabolomics results discovered that 11 different metabolites in rats and 20 different metabolites in DVT patients. Seven metabolites both altered in the rats and patients. Moreover, we observed changes in the metabolic pathways, including carbohydrate metabolism, lipid metabolism, and amino acid metabolism that were induced immediately by the thrombosis. Pathway of aminoacyl-tRNA biosynthesis perturbed only in the patients which was associated with the genetic risk factor of DVT. The study demonstrated that serum 1H NMR metabolomics can be used to diagnose DVT in the clinic. The altered pathways related to thrombosis and genetics will provide a foundation and new strategies for understanding the pathological mechanism and pharmacological targets of DVT.

/pdf/comparison-of-the-serum-metabolic-signatures-based-on-1h-nmr-2a4iiiari1.pdf

Comparison of the serum metabolic signatures based on 1H NMR between patients and a rat model of deep vein thrombosis.

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Comparison of the serum metabolic signatures based on 1H NMR between patients and a rat model of deep vein thrombosis.