Hepatic steatosis in waterfowl

The fatty liver of overfed waterfowl results from a hepatic steatosis induced by specific nutritional conditions. This steatosis is hypertrophic, reversible and characterised by an accumulation of triglycerides in the hepatocytes. This ability is favoured by different physiological and metabolic peculiarities of birds such as the main site of lipid synthesis which is the liver and the use of a specific feed, maize rich in starch and distributed in large quantities to waterfowl. This important amount of maize stimulates two transcription factors regulated respectively by insulin, SREBP-1c and by glucose, ChREBP which will act then on glycolysis and lipogenesis. However, the ability to produce fatty liver depends on species and even the genotype of waterfowl. It results essentially from an increased capacity of hepatic lipogenesis, an insufficient hepatic capacity to export neo synthesised triglycerides and a limited capacity of peripheral tissues in the uptake of circulating lipids then favouring their return towards the liver and therefore increasing the development of steatosis. The selection on the weight of fatty liver is effective. Three QTL controlling the weight of fatty liver of the mule duck were detected on chromosomes 2, 9 and 21 of the common female duck. In addition with adapted rearing and feeding conditions, geese are able to initiate a spontaneous hepatic steatosis. This constitutes a perspective to developing fatty liver production without using overfeeding.