AI Article Synopsis

  • Different duck species, specifically Muscovy and Pekin ducks, show variations in their likelihood to develop hepatic steatosis, potentially due to differences in how they metabolize fats or respond to overfeeding.
  • A study found that Muscovy ducks had significantly higher rates of lipogenesis from glucose and uptake of linoleic acid compared to Pekin ducks, indicating more intense fat metabolism.
  • Despite the higher secretion of VLDL (a type of fat carrier) in Muscovy ducks, it was still not enough to prevent fat buildup in their livers, highlighting key differences in liver metabolism that could inform human studies on fatty liver disease.

Article Abstract

The susceptibility to develop hepatic steatosis is known to differ between duck species, especially between Muscovy and Pekin ducks. This difference could be explained by either differential responses of species to overfeeding or genetic differences in hepatic lipid metabolism. The aim of the present study was to compare the intensities of the different hepatic pathways (oxidation, lipogenesis, esterification, secretion, etc.) of the two main nutrients (glucose and linoleic acid (LA)) reaching the liver of ad libitum-fed Muscovy (n 6) and Pekin (n 6) ducks using the ex vivo method of liver slices incubated for 16 h with [U-14C]glucose, [1-14C]LA and [35S]methionine added to the survival medium. In such experimental conditions, the lipogenesis pathway from glucose was 2-fold higher (P<0.05) in the liver of the Muscovy duck than in that of the Pekin duck. Furthermore, the hepatic uptake of LA was 2-fold higher (P<0.05) in the Muscovy duck than in the Pekin duck leading to a 2-fold higher (P<0.05) esterification of this fatty acid in the liver of the Muscovy duck. The hepatic secretion of VLDL was higher (P<0.01) in the Muscovy duck than in the Pekin duck but insufficient to prevent lipid accumulation in the liver of the Muscovy duck. In conclusion, these results show the influence of the species on the hepatic metabolism of ducks in relation to their susceptibility to develop fatty liver. These results should shed light on the metabolic regulations that might underlie susceptibility to hepatic steatosis in the the human liver.

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Source
http://dx.doi.org/10.1017/S0007114508019892DOI Listing

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