Plasma lipoproteins and liver lipids in two breeds of geese with different susceptibility to hepatic steatosis: Changes induced by development and force‐feeding

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Abstract
Susceptibility to fatty liver in the force‐fed goose is partly under genetic control. However, the mechanisms leading to liver steatosis in this avian model are poorly understood, but may involve perturbation in hepatic lipoprotein synthesis. Plasma lipoproteins were fractionated by density gradient ultracentrifugation from plasma of geese differing in their susceptibility to liver steatosis (Landes breed, highly susceptible; Rhine breed, partly resistant). The concentrations and chemical compositions of the major lipoprotein classes (VLDL, IDL, LDL and HDL) were characterized at 8, 22 and 27 wk of age and compared to the lipid composition of the corresponding liver. In non‐force‐fed geese, the lipoprotein profile was typical of birds, with high‐density lipoprotein (HDL) predominating (4–5 g/L). However, at 22 and 27 wk of age, very low‐density lipoprotein (VLDL) levels were significantly lower in Landes geese suggesting that this breed may possess a lower ability to export liver lipids, which would explain its susceptibility to liver steatosis when overfed. The livers of force‐fed geese were specifically enriched in triglyceride, and to a lesser extent, in cholesteryl esters and non‐esterified fatty acids as compared to those of control geese of the same age (27 wk). This accumulation of lipids was more pronounced in the Landes breed and was responsible for the higher liver weight in that breed. In both breeds, liver steatosis was accompanied by an increase in plasma levels of HDL (11 g/L), whereas low‐density lipoproteins were essentially absent. An increase in VLDL plasma levels occurred in the Landes breed only (2.51 g/Lvs 1.85 g/L in the Rhine breed), and was positively correlated with liver weight. However, VLDL in force‐fed geese in both breeds were deficient in triglyceride (28–29% by wt) but enriched in cholesterol (41% by wt). These results indicate that a defect in the incorporation of triglyceride into nascent hepatic VLDL may result in liver steatosis in this species.