Abstract
Chronic excessive alcohol consumption is associated with multiple liver defects, such as steatosis and cirrhosis, mainly attributable to excessive reactive oxygen species (ROS) production. Barley sprouts (Hordeum vulgare L.) contain high levels of polyphenols that may serve as potential antioxidants. This study aimed to investigate whether barley sprouts extract powder (BSE) relieves alcohol-induced oxidative stress and related hepatic damages in habitual alcohol drinkers with fatty liver. In a 12-week randomized controlled trial with two arms (placebo or 480 mg/day BSE; n = 76), we measured clinical markers and metabolites at the baseline and endpoint to understand the complex molecular mechanisms. BSE supplementation reduced the magnitude of ROS generation and lipid peroxidation and improved the glutathione antioxidant system. Subsequent metabolomic analysis identified alterations in glutathione metabolism, amino acid metabolism, and fatty acid synthesis pathways, confirming the role of BSE in glutathione-related lipid metabolism. Finally, the unsupervised machine learning algorithm indicated that subjects with lower glutathione reductase at the baseline were responders for liver fat content, and those with higher fatigue and lipid oxidation were responders for γ-glutamyl transferase. These findings suggest that BSE administration may protect against hepatic injury by reducing oxidative stress and changing the metabolism in habitual alcohol drinkers with fatty liver.
Highlights
Alcohol-related deaths account for 5.3% of all deaths worldwide [1]
The results indicated that the subjects with a baseline GR activity lower or equal to 141.9 nmol/min/mL were responders (Leaf 1, n = 28) whose liver fat content was significantly reduced by barley sprouts extract powder (BSE) supplementation compared with the placebo group (p = 0.003)
The results indicated that the subjects with fatigue severity score (FSS) (Leaf 2, n = 51), reactive oxygen species (ROS) AUC (Leaf 2, n = 54), or ox-LDL (Leaf 2, n =51) values higher than the corresponding split points were responders whose generation may also enhance γ-glutamyl transferase (GGT) levels were remarkably reduced by BSE supplementation compared with the placebo group
Summary
Many factors are involved in the pathogenesis of alcoholic liver disease, including alcohol metabolism-associated oxidative stress and abnormal glutathione (GSH) metabolism [3]. The liver is the primary site where alcohol is oxidized to acetaldehyde by alcohol dehydrogenase (ADH) in the cytosol, cytochrome P450 2E1 (CYP2E1) in the microsome, and catalase (CAT) in the peroxisomes [4]. Increased expression of CYP2E1 generates excessive reactive oxygen species (ROS) [5], leading to the peroxidation of membrane lipids and proteins, inflammation, and insulin resistance, which may, in turn, favor the development of hepatic steatosis [6,7,8,9,10]. Alcohol-induced excessive ROS generation may enhance γ-glutamyl transferase (GGT) release from the damaged hepatocellular membrane [11]
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