Comparative metabolomic profiling reveals distinct patterns between patients with alcoholic liver disease and non-alcoholic fatty liver disease, suggesting metabolic alterations.
Aim: to investigate the metabolomic profile of patients with alcoholic liver disease and non-alcoholic fatty liver disease. Materials and methods. The present study included patients diagnosed with non-alcoholic fatty liver disease (NAFLD) ( n = 44), patients diagnosed with alcoholic liver disease (ALD) ( n = 40) and 14 healthy volunteers. The level of metabolites in the blood serum were determined via high-performance liquid chromatography and tandem mass spectrometry. Results. In this study, a cross-sectional targeted metabolomic analysis of 96 serum metabolites was performed in patients. Statistical analysis using the principal component method identified six main factors, comprising metabolites from various metabolic pathways. Comparative analysis between patient groups and the control group revealed statistically significant differences in the metabolic activity of individual factors, collectively reflecting alterations in the metabolomic profile. Levels of acylcarnitines, uridine, metanephrine, asymmetric and total dimethylarginine were elevated in patients with NAFLD and ALD compared to the control group. Carnitine, short chain acylcarnitines, valine, leucine, lysine, and alanine were significantly higher in patients with NAFLD compared to those with ALD. In contrast, levels of tyrosine, epinephrine, and methionine were significantly increased in ALD patients compared to both NAFLD patients and healthy volunteers. Among patients with liver cirrhosis (both ALD and NAFLD), there was a noticeable trend toward altered metabolic activity of factors correlating with liver failure indicators and the FIB-4 index. As liver cirrhosis progressed, statistically significant changes in metabolite levels were observed across Child — Pugh classes, taking into account hypocoagulation, hypoalbuminemia, hyperbilirubinemia, the presence of ascites, and hepatic encephalopathy.
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Reshetova et al. (2025) studied this question.
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