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  • Insulin effect on lipogenesis and fat distribution in three genotypes of ducks during overfeeding.

Insulin effect on lipogenesis and fat distribution in three genotypes of ducks during overfeeding.

Comparative biochemistry and physiology. Part A, Molecular & integrative physiology (2013-01-03)
Karine Gontier, Jean-Marc André, Marie-Dominique Bernadet, Karine Ricaud, Stéphane Davail
摘要

In waterfowl, the response to overfeeding differs from one genotype to the other. Pekin ducks generally store lipids in the peripheral tissues while Muscovy and mule ducks promote hepatic lipid storage. A possible reason for these various susceptibilities to hepatic steatosis could be a difference in insulin sensitivity. We suggest a resistance to insulin in Pekin ducks. In the present work we investigate the action of insulin on glucose and lipid metabolisms for the three overfed genotypes. Regardless of the kind of genotype, all ducks appear to be sensitive to insulin: their glycemia is lower when the animals are treated with insulin. Insulin-treated Muscovy and Pekin ducks present a lower increase in total body weight (-16.5% for Muscovy; -8.3% for Pekin); and a significantly lower liver weight than the controls (-9.6% and -18.3%). The percentage of total lipids in the liver is higher in the controls than in the insulin-treated Pekin and mule ducks (respectively -40.4% and -34.7%), which means a decreased hepatic lipogenesis. Pekin ducks present a higher pectoral muscle weight when the individuals are insulin-treated (+9.7%). Lipoprotein lipase (LPL) activity appears to be significantly higher in insulin-treated Pekin and Muscovy ducks (1.39 and 3.38 times greater than controls). Insulin-treated mule ducks present a decrease of muscle and abdominal lipid storage compared to controls (-11.6% and -13.8%). In this experiment, exogenous insulin has induced an increase of lipid oxidation and has led to a less favorable use and storage of dietary glucose. The hypothesis of insulin-resistance of Pekin ducks is not verified.

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Sigma-Aldrich
脂蛋白脂肪酶 来源于假单胞菌 属, lyophilized, powder, ≥1200 U/mg
Sigma-Aldrich
脂蛋白脂酶 来源于伯克霍尔德氏菌 属, lyophilized powder, ≥50,000 units/mg solid
Sigma-Aldrich
脂蛋白脂酶 来源于牛奶, ammonium sulfate suspension, ≥2,000 units/mg protein (BCA)
Sigma-Aldrich
脂蛋白脂肪酶 来源于假单胞菌 属, lyophilized, powder, yellow-brown, ≥160 U/mg