INFLUENCE OF EROTIC ACID AND ESTROGEN ON HEPATIC LIPID STORAGE AND SECRETION IN THE GOOSE SUSCEPTIBLE TO LIVER STEATOSIS

Fatty liver in the goose results from an increased hepatic lipogenesis in response to overfeeding, together with a deficient secretion of tr iacylglycerol as very-low-density lipoproteins (VLDL). Orotic acid and estrogen, which both modify lipid metabolism in the liver, were used in male geese as tools to understand the alterations of liver lipids a nd plasma lipoproteins during the induction of liver steatosis. Liver lipids were analyzed after solvent extraction and plasma lipoproteins after separation by density gradient ultracentrifugation. Contrary to what is known in the rat, erotic acid (1% in food for 2 weeks) failed to induce liver steatosis. In force-fed geese, liver weight increased from approximate to 100 g to approximate to 800 g in 2 weeks, as a con sequence of a specific accumulation of triacylglycerol; In both groups , VLDL contained less triacylglycerol (35%) than normal. Such an uncou pling of triacylglycerol synthesis and secretion, of which the precise reason is still unknown, may facilitate their accumulation when force -feeding increases hepatic lipogenesis. As with force-feeding, triacyl glycerol synthesis was enhanced by estrogen, but their secretion as VL DL was very efficient and prevented liver steatosis almost completely. Since HDL concentrations were considerably decreased by estrogen, VLD L were the main lipoprotein species, with 48 g/l and 62% triacylglycer ol. Where estrogen-treated geese were force-fed concomitantly, VLDL co ncentration was even higher (62 g/l), but triacylglycerol secretion co uld not prevent liver steatosis (liver weight 640 g). The data are dis cussed in relation to in vitro studies showing that channelling of tri acylglycerol towards secretion as VLDL or hepatic storage depends on t heir residence time in the different intracellular compartments.