Avian fatty liver hemorrhagic syndrome: a comparative review

Abstract

Metabolic fatty liver syndromes occur in a variety of species including chickens, humans, cows, and cats. Both energy excess and deficit appear to initiate the accumulation of liver fat. Although the conditions preceding the onset of liver steatosis vary, all syndromes share a common basis in altered lipid utilization, lipoprotein assembly, and secretion. Laying hens and humans appear to develop fatty livers under similar metabolic conditions of energy excess. This similarity and the additional structural requirements inherent in yolk deposition make the laying hen an exciting model in which to study lipoprotein synthesis, assembly, and secretion. The overfed hen provides additional insights into the effects of nutrition and hormones on these same processes. Within this model it may be possible to distinguish the effects of altered gene expression versus altered physical properties (lipids) and postranslational processing (proteins) in mediating the observed responses.