RELATIONSHIPS BETWEEN STORAGE AND SECRETION OF HEPATIC LIPIDS IN 2 BREEDS OF GEESE WITH DIFFERENT SUSCEPTIBILITY TO LIVER STEATOSIS

Citation
E. Fournier et al., RELATIONSHIPS BETWEEN STORAGE AND SECRETION OF HEPATIC LIPIDS IN 2 BREEDS OF GEESE WITH DIFFERENT SUSCEPTIBILITY TO LIVER STEATOSIS, Poultry science, 76(4), 1997, pp. 599-607
Citations number
24
Categorie Soggetti
Agriculture Dairy & AnumalScience
Journal title
ISSN journal
00325791
Volume
76
Issue
4
Year of publication
1997
Pages
599 - 607
Database
ISI
SICI code
0032-5791(1997)76:4<599:RBSASO>2.0.ZU;2-S
Abstract
Susceptibility to liver steatosis was studied in Landes and Poland gee se, which are hyper- and hyporesponsive, respectively, to overfeeding. Plasma lipoproteins were characterized at different stages of the ove rfeeding process, whereas fatty liver composition was determined after completion of overfeeding and slaughtering. Before overfeeding, plasm a lipoprotein profile was typical of birds in both breeds, except that very low density lipoproteins (VLDL) were low in triglyceride (simila r to 30%). Moreover, high-density lipoprotein (HDL) concentration was higher in the Poland geese (6.44 vs 4.97 g/L). During overfeeding, hep atic Lipogenesis was increased, and fatty liver resulted from accumula tion of primarily triglyceride (similar to 95% of lipid content), but also of all other lipids. This accumulation was significantly greater in the Landes geese for all Lipids but phospholipid. Thus, the liver w eight was 100% higher in this breed (1,005 g vs 485 g), whereas lipid release during sterilization was twofold higher (26.3 vs 7.5%). Parall ely, plasma concentration and triglyceride content of hepatic lipoprot eins, VLDL and HDL, increased about one- to twofold, this effect being greater in the Poland geese. Therefore, channeling of triglyceride to wards secretion rather than in situ storage may be responsible for the hyporesponsiveness of this breed to overfeeding. In both breeds, and especially in the Landes geese, a relative deficiency in phospholipid synthesis together with an enhanced secretion may be limiting factors of hepatocyte hypertrophia and, therefore, of steatosis.