Precursors such as uridine diphosphate (UDP), UDP-N-acetyl-D-glucosamine, or glucosamine are used to synthesize galactosamine in the human body.

The result of using galactosamine to induce hepatitis is a disease model in which there is necrosis and inflammation of the liver.

This type of tissue damage triggered by galactosamine resembles drug-induced liver disease in humans.

Additionally, other derivatives of uridine such as UDP-glucose are depleted and this interferes with glycogen synthesis in the cell.

Another recent hypothesis states that overexpression of pro-inflammatory cytokines (such as tumor necrosis factor (TNFα) and NFκB-dependent inducible nitric oxide synthase (iNOS) over expression play a role in galactosamine-induced damage to liver cells.