Abstract
Mule ducks have been force-fed to develop a hepatic steatosis, also called "foie gras", which is similar to the non-alcoholic fatty liver disease (NAFLD) described in humans and mammals. However, in hepatic steatosis resulting from force-feeding of ducks, very little is known about the fine biochemical events that occur due to the enormous and very rapid increase in total lipids that mainly accumulate in hepatocytes. To begin to reduce this lack of knowledge associated with the development of this specific hepatic steatosis, liver samples were taken at different times to follow the overall biochemical transformation of the liver as well as different markers of oxidative stress, hypoxia and apoptosis. The results indicate that the lipid content increases rapidly in the liver throughout the force-feeding period while the protein content decreases. The amount of hydroxyproline remains constant indicating that no liver fibrosis develops during the force-feeding period. On the contrary, all the tested biomarkers of cellular oxidative stress increase rapidly but without any visible disorder in the coordination of paired activities. At the same time, hypoxia-inducible factors also increase indicating that a hypoxia situation is gradually occurring in hepatocytes. This leads, in addition to the lipotoxicity induced by the accumulation of lipids, to an increased number of liver cells to enter into apoptosis. A relative variability in the level of these cellular responses was also observed indicating that, probably, certain animals support the development of this steatosis differently. This leads us to imagine that the physiological status of these birds may differ widely for reasons that remain to be clarified.