Current understanding of the metabolism of micronutrients in chronic alcoholic liver disease

Table 1 Micronutrients imbalance in patients with alcoholic liver disease

Micronutrient	Metabolic status	Effects	Potential mechanisms	Ref.
Zinc	Deficiency	Intracellular signaling transduction, inflammatory response, ROS production, immunoregulation	Decreases tight-junction proteins, increases the risk of intestinal barrier dysfunction; Inhibition of oxidative stress; Disturbs dendritic cells’ ability to respond to LPS; Activates apoptosis	[15,17,24]
Iron	Overload	Controls the transportation of oxygen; DNA biosynthesis; ATP synthesis	Activates HSC, promoting liver fibrosis; Induces ferroptosis and mitochondrial dysfunction; Provokes oxidative damage through the Fenton reaction; influences myelination and neurotransmitters	[34-37,43,45]
Copper	Deficiency/ overload	The precise function of bone marrow and the central nervous system; A cofactor of many antioxidases	Interacts with other trace elements, and functions as a cofactor of antioxidases responsible for antioxidant defense	[48-51]
Selenium	Deficiency	Antioxidant property	Increases the enzyme activity of glutathione peroxidase and protects against oxidative injury; participates in autophagy, caspase-involved apoptosis, and NF-kB-implicated inflammation regulation	[52,55-58]
Magnesium	Deficiency	Participates in enzymatic reactions, neurotransmission, glycolysis, and mitochondrial function	Perturbs the extrusion of cellular magnesium in a Na+-dependent and Na+-independent manner	[66-68]
Vitamin D	Deficiency	Anti-fibrosis, anti-tumor, and anti-inflammation; Immunomodulation	Not yet fully understood	[73,74]
Vitamin E	Deficiency	Antioxidative properties; protects against hepatocyte necrosis and maintains mitochondrial integrity	Diminishes alcohol-induced oxidative damage, and improves antioxidant defense; Regulates the EGFR-AKT and EGFR-STAT3 pathways	[84,88-90]

ALD: Alcoholic liver disease; ROS: Reactive oxygen species; DNA: Deoxyribonucleic acid; HSC: Hepatic stellate cells.