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

A derivative of this compound is N-acetyl-D-galactosamine.

Hepatotoxicity
Galactosamine is used to induce hepatitis in rodent liver for research purposes. 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.

Mechanism of Hepatotoxicity
The proposed mechanism behind galactosamine-induced hepatitis is depletion of the energy source of hepatocytes. In the Leloir pathway galactosamine is metabolized into galactosamine-1-phosphate (by galactokinase) and UDP-galactosamine (by UDP-galactose uridyltransferase). It is hypothesized that this leads to UDP-galactosamine accumulation within cells, and uridine triphosphate (UTP), UDP, and UMP) decrease . The depletion of high-energy molecules such as UTP leads to a disruption in hepatocyte metabolism. 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 TNFα) and NFκB dependent iNOS over expression play a role in galactosamine-induced damage to liver cells.