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首页> 外文期刊>American Journal of Physiology >Kinetic study of the expression of genes related to hepatic steatosis, glucose and lipid metabolism, and cellular stress during overfeeding in mule ducks
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Kinetic study of the expression of genes related to hepatic steatosis, glucose and lipid metabolism, and cellular stress during overfeeding in mule ducks

机译：骡鸭肝脏脂肪变性，葡萄糖和脂质代谢相关基因表达的动力学研究及细胞应激

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摘要

Induced by overfeeding, hepatic steatosis is a process exploited for the "foie gras" production in mule ducks. To better understand the mechanisms underlying its development, the physiological responses of mule ducks overfed with corn for a duration of 11 days were analyzed. A kinetic analysis of glucose and lipid metabolism and cell protection mechanisms was performed on 96 male mule ducks during overfeeding with three sampling times (after the 4th, the 12th, and the 22nd meal). Gene expression and protein analysis realized on the liver, muscle, and abdominal fat showed an activation of a cholesterol biosynthetic pathway during the complete overfeeding period mainly in livers with significant correlations between its weight and its cholesterolemia (r = 0.88; P < 0.0001) and between the liver weight and the hmgcr and soat1 expression (r = 0.4, P < 0.0001 and r = 0.67; P < 0.0001, respectively). Results also revealed an activation of insulin and amino acid cells signaling a pathway suggesting that ducks boost insulin sensitivity to raise glucose uptake and use via glycolysis and lipogenesis. Cellular stress analysis revealed an upregulation of key autophagy-related gene expression atg8 and sqstm1(P < 0.0001) during the complete overfeeding period, mainly in the liver, in contrast to an induction of cyp2e1(P < 0.0001), suggesting that autophagy could be suppressed during steatosis development. This study has highlighted different mechanisms enabling mule ducks to efficiently handle the starch overload by keeping its liver in a nonpathological state. Moreover, it has revealed potential biomarker candidates of hepatic steatosis as plasma cholesterol for the liver weight.
机译：通过过度灌注诱导，肝脏脂肪变性是在骡子鸭的“鹅肝”产生的过程中。为了更好地了解其发展的基础，分析了玉米持续时间持续11天的龙鸭的生理反应。在用三次取样时间（第4次，第12次和第22次之后，在96只雄骡子鸭肉进行了葡萄糖和脂质代谢和细胞保护机制的动力学分析。在肝脏，肌肉和腹部脂肪上实现的基因表达和蛋白质分析显示，在完全过度的过度期间，主要在肝脏的完全过度期间激活胆固醇生物合成途径，其重量与其胆固醇血症之间具有显着相关性的（r = 0.88; p <0.0001）和在肝脏重量和HMGCR和SOAT1表达之间（r = 0.4，p <0.0001和r = 0.67; p <0.0001）。结果还揭示了胰岛素和氨基酸细胞的激活，所述途径表明鸭子促进胰岛素敏感性，以通过糖酵解和脂肪生成来升高葡萄糖摄取和使用。细胞应激分析显示，在完全过度喂养期间，主要在肝脏中的关键自噬相关基因表达ATG8和Sqstm1（P <0.0001）的上调，与CYP2E1的诱导相比，暗示自噬可以是在脂肪变性发展期间抑制了。该研究突出了不同机制，使骡子鸭通过保持其肝脏以非流通状态而有效地处理淀粉过载。此外，它揭示了肝硬化的潜在生物标志物候选者，作为肝脏重量的血浆胆固醇。

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