Increased fat synthesis and limited apolipoprotein B cause lipid accumulation in the liver of broiler chickens exposed to chronic heat stress
Increased fat synthesis and limited apolipoprotein B cause lipid accumulation in the liver of broiler chickens exposed to chronic heat stress
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DOI：
10.3382/ps/pez056
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发表时间：
2019-09-01
期刊：
影响因子：
4.4
通讯作者：
Gao, F.
中科院分区：
文献类型：
--
作者：
Lu, Z.;He, X. F.;Gao, F.
慢性热应激可促进肉鸡脂肪合成，肝脏合成的过量甘油三酯（TG）需要通过极低密度脂蛋白（VLDL）转运至肝外组织，否则会在肝脏内蓄积，甚至导致肝脏脂肪变性。为了研究慢性热应激促进鸡肝脏脂肪合成并导致脂质积累的分子机制，将144只肉鸡（Arbor Acres，28日龄）随机分为正常对照组（NC，22 ℃）、热应激组（HS，一致32 ℃）和配对饲养组（PF，22 ℃）进行14-D试验。7 D热暴露显著增加了呼吸频率、腹脂相对重量、血浆中葡萄糖、甘油三酯、皮质酮、胰岛素和极低密度脂蛋白水平，以及肝脏中甘油三酯、总胆固醇、酰基辅酶A羧化酶（ACC）和脂肪酸合成酶（FAS）水平，和微粒体甘油三酯转运蛋白（MTTP）。热暴露14 D后，HS组腹脂和肝脏相对重量、肝脏TG和FAS水平显著高于其他2组，而3组间呼吸频率、血浆皮质酮浓度、肝脏载脂蛋白B（ApoB）水平和脂肪合成关键基因mRNA表达水平无显著差异。总之，慢性热暴露激活LXR α通路，并在热暴露7天后增强肝脏中的脂肪合成。热暴露14 D后，热应激肉鸡在应激参数和脂肪合成基因表达水平上表现出对高温的适应。此外，慢性热应激导致肉鸡肝脏脂质蓄积，这可能是由于慢性热应激肉鸡体内有限的ApoB不足以转运肝脏合成的过量TG所致。
Chronic heat stress can enhance fat synthesis in broilers, and excessive triglyceride (TG) synthesized by the liver needs to be transported to extrahepatic tissues by very low density lipoprotein (VLDL) otherwise will accumulate in the liver, which may even result in hepatic steatosis. To investigate the molecular mechanisms by which chronic heat stress enhances fat synthesis and results in lipid accumulation in the liver of chickens, 144 broilers (Arbor Acres, 28-day-old) were randomly allocated to the normal control (NC, 22 degrees C), heat stress (HS, consistent 32 degrees C), or pair-fed (PF, 22 degrees C) groups for a 14-D trial. The 7 D of heat exposure significantly increased the respiratory rate, relative weight of abdominal fat, the levels of glucose, TG, corticosterone, insulin, and VLDL in plasma, as well as the levels of TG, total cholesterol, acyl-CoA carboxylase (ACC), and fatty acid synthase (FAS) in the liver, and mRNA expression levels of carbohydrate response element-binding protein (ChREBP), ACC, FAS, and microsomal triglyceride transfer protein (MTTP) in comparison with the other 2 groups. After 14 D of heat exposure, the relative weights of abdominal fat and liver and levels of TG and FAS in the liver were significantly higher in the HS group than in the other 2 groups, and there were no significant differences in the respiratory rate, plasma corticosterone concentration, apolipoprotein B (ApoB) level in the liver, and mRNA expression levels of key genes of fat synthesis among the 3 groups. In conclusion, chronic heat exposure activated LXRa pathway and enhanced fat synthesis in the liver after 7 D of heat exposure. After 14 D of heat exposure, heat-stressed broilers exhibited an adaptation to the high temperature in parameters of stress and fat synthesis gene expression levels. Moreover, chronic heat stress resulted in lipid accumulation in the liver of broilers, which is probably because the limited ApoB was not enough to transport the excessive TG synthesized by the liver in chronic heat-stressed broilers.