Energy Availability and Alcohol-Related Liver Pathology

Alcohol consumption alters the metabolism of the most common type of cell found in the liver, the hepatocyte. The presence of alcohol in the body causes the liver to use more oxygen—for example, when breaking down the alcohol. Increased oxygen use, in turn, causes oxygen deficits in several key cells, particularly in hepatocytes located near the small hepatic veins. These veins return blood to the heart for re-oxygenation after it has passed through the liver. Hepatocytes surrounding these veins are the first to show signs of liver disease. The damage induced by oxygen deficits may be exacerbated by alcohol-induced deficits in other components that are essential for cell survival. For example, adenosine triphosphate (ATP), the cell’s main source of energy, is generated primarily during the course of two sets of metabolic reactions: glycolysis and the mitochondrial oxidative phosphorylation process. Alcohol consumption may interfere with both of these pathways of ATP production through several mechanisms. An inadequate supply of ATP impairs the cell’s ability to perform critical functions, including the repair of alcohol-induced cell damage, and may therefore contribute to cell death and alcoholic liver disease.