Abstract
Alcoholic liver disease (ALD) as a consequence of ethanol chronic consumption could lead to hepatic cirrhosis that is linked to high morbidity and mortality. Disease diagnosis is still very challenging and usually clear findings are obtained in the later stage of ALD. The profound effect of ethanol on metabolism can be depicted using metabolomics; thus, the discovery of novel biomarkers could shed light on the initiation and the progression of the ALD, serving diagnostic purposes. In the present study, Hydrophilic Interaction Liquid Chromatography tandem Mass Spectrometry HILIC-MS/MS based metabolomics analyisis of urine and fecal samples of C57BL/6 mice of both sexes at two sampling time points was performed, monitoring the effect of eight-week ethanol consumption. The altered hepatic metabolism caused by ethanol consumption induces extensive biochemical perturbations and changes in gut microbiota population on a great scale. Fecal samples were proven to be a suitable specimen for studying ALD since it was more vulnerable to the metabolic changes in comparison to urine samples. The metabolome of male mice was affected on a greater scale than the female metabolome due to ethanol exposure. Precursor small molecules of essential pathways of energy production responded to ethanol exposure. A meaningful correlation between the two studied specimens demonstrated the impact of ethanol in endogenous and symbiome metabolism.
Highlights
Chronic consumption of ethanol is a leading cause of alcohol liver disease (ALD)
This study aimed to investigate the effect of ethanol on the metabolic content of urine and fecal samples in a mouse model simulating chronic exposure to ethanol
The applied protocol lasted for a period of eight weeks, urine and fecal samples presented in this work were collected up until the 20th day of exposure
Summary
Chronic consumption of ethanol is a leading cause of alcohol liver disease (ALD). As this implication is the far end of intermediate and reversible stages characterized by hepatic steatosis, which is caused by lipid metabolism dysregulation mechanisms triggered by ethanol, early diagnosis of detrimental ethanol consumption is of high significance. The diagnosis of ALD can be clinically challenging as there is no single test that confirms the presence of the disease and patients may not always provide clear information concerning their alcohol consumption patterns. The development of noninvasive tests based on metabolic markers indicative of early stage ALD could augment the power of regular tests, improving the potential for early detection of ethanol toxic effects and promoting measures toward disease prevention [2,3]
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