Molecular effects of alcohol on iron metabolism

This chapter explores the link between iron and alcohol metabolism. Chronic alcohol consumption alters the expression of numerous iron-related proteins, including the liver-secreted systemic iron-regulator hepcidin. Downregulation of hepcidin is the key reason for increased duodenal iron absorption, which causes high circulating and stored iron levels in alcoholics, similar to that attained in hereditary hemochromatosis. The resultant free-iron mediated cytotoxicity is a common determinant of the pathophysiology of cirrhosis, an advanced liver condition observed in both alcoholic liver disease (ALD), and congenital hemochromatosis. Often, alcohol consumption suppresses hematopoiesis and/or hinders normal erythrocyte maturation, which results in anemia. Due to these alcohol-induced changes in iron metabolism, several iron-related biomarkers, like serum levels of ferritin and the glycosylation status of transferrin, are used to detect ALD. Also, modulation of hepcidin expression has been explored as a therapy to limit duodenal iron absorption and thereby restrain the tissue injury mediated by excess iron.