In mature hens of the domesticated chicken (Gallus gallus), accumulation of yolk is predominantly the result of massive macromolecular transport. Yolk is mainly comprised of lipid-rich complexes produced in the liver of the laying hen (LH) and secreted in the form of yolk precursors, which are directed towards the oocyte.
Lipid homeostasis of somatic tissues must be maintained, a process that is partly achieved through the regulation of systemic lipoprotein metabolism involving lipases. In mammals, intracellular lipolysis of triacylglycerol (TG) to fatty acids and glycerol is mediated by the sequential action of adipose TG lipase (ATGL), hormone sensitive lipase (HSL), and monoacylglycerol lipase (MGL). An ortholog of HSL has to date evaded attempts to be identified. In this thesis, several approaches to identify an HSL homolog in chicken were performed; however, its existence could not be demonstrated. I extended these studies to arylacetamide deacetylase (AADA). Here, I describe the implication of AADA in chicken hepatic lipid metabolism, and compare its regulation to that of galline ATGL (ggATGL) and the galline protein patatin-like phospholipase domain-containing lipase 3 (ggPNPLA3). In this thesis I show that AADA is predominantly expressed in the liver. I further show that galline heptic AADA, ATGL and PNPLA3 are regulated by the nutritional state and that hepatic expression of chicken AADA is estrogen-responsive, and is induced to the same degree as the stimulation of VLDL-production by estrogen. Additionally, the enzyme appears to colocalize with cytoplasmic lipid-rich structures that may represent possibly ER-associated lipid droplets.