Unravelling fatty liver haemorrhagic syndrome: 1. Oestrogen and inflammation
Previous studies have implicated oestrogen as a factor in the induction of fatty liver haemorrhagic syndrome (FLHS). In this study, a refined laying hen model was employed to permit further investigations. Intramuscular (i.m.) injections of exogenous oestrogen as β-estradiol-17-dipropionate (E2) (5 mg/kg BW) were given every 4 days for 20 days to 30-week-old hens fed either ad libitum or with restricted feed intake. Elevated (P < 0.01) plasma oestrogen concentrations produced significant macroscopic and microscopic hepatic alterations. Hens in the E2-treated ad libitum fed (EAL) group experienced a higher incidence of FLHS than hens in the E2-treated restricted feed intake group, showing that birds with a higher feed intake are more at risk of developing FLHS. Histological examination of livers revealed that hens in the E2-treated ad libitum fed group had consistent and severe fat infiltration in the liver, and fat vacuolization within hepatocytes. Fat accumulation and fat droplets were found not only in the cytoplasm of hepatocytes but also in liver sinusoids. White blood cell counts and fibrinogen concentrations were altered (P < 0.01) in hens treated with E2 when compared with controls. Plasma fibrinogen concentrations were altered over time, and correlated with white blood cell counts (Pearson’s correlation r = 0.96; P = 0.001). Hens treated with E2 had increased (P < 0.01) levels of cholesterol and triglycerides, confirming that E2 induced hypercholesterolaemia and hypertriglyceridaemia. It was concluded that E2 successfully induced FLHS in hens, with typical systemic and hepatic events resulting from a disturbance in lipid metabolism and chronic low-grade inflammation.
