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地塞米松诱导氧化应激的鸡的糖脂代谢紊乱

Glucose and lipid metabolism disorders in the chickens with dexamethasone-induced oxidative stress.

作者信息

Lv Z-P, Peng Y-Z, Zhang B-B, Fan H, Liu D, Guo Y-M

机构信息

State Key Laboratory of Animal Nutrition, College of Animal Science & Technology, China Agricultural University, Beijing, China.

出版信息

J Anim Physiol Anim Nutr (Berl). 2018 Apr;102(2):e706-e717. doi: 10.1111/jpn.12823. Epub 2017 Nov 3.

DOI:10.1111/jpn.12823
PMID:29098735
Abstract

The purpose of this study was to investigate the effects of long-term treatment with dexamethasone (DEX) on the antioxidation and nutrition metabolism in broiler chickens. Broilers were placed on a high-nutrient diet for 41 days, and half were given orally DEX-supplemented water at 20 mg/L every other day from 19 to 41 days of age. DEX treatment downregulated superoxide dismutase activity as well as the mRNA expression of CuZn-superoxide dismutase and glutathione peroxidase with a decrease in GSH/GSSG ratio and an increase in malondialdehyde level in the liver of broilers. DEX treatment aggravated oxidative damage in the liver and, therefore, increased the sensitivity of broilers to ascites syndrome with higher mortality and reduced growth performance. Serum metabolomics analysis showed that DEX treatment significantly increased the levels of glucose, intermediates in protein metabolism (valine, proline, serine, threonine and urea) and lipid metabolism-related products (palmitic acid, stearic acid and cholesterol) while decreasing the levels of β-hydroxy butyric acid, succinic acid and malic acid, demonstrating that DEX treatment inhibited the Krebs cycle and the oxidation of fatty acids, and promoted the de novo synthesis of fatty acids as well as protein decomposition in the liver of broilers. Additionally, detection of metabolism-related enzymes revealed that DEX treatment inhibited glycolysis and promoted glycogen decomposition. In summary, DEX treatment resulted in oxidative stress and glucose and lipid metabolism disorders in the broilers.

摘要

本研究旨在探讨地塞米松(DEX)长期治疗对肉鸡抗氧化和营养代谢的影响。将肉鸡置于高营养日粮饲养41天,其中一半从19日龄至41日龄每隔一天口服含20 mg/L DEX的水。DEX处理下调了肉鸡肝脏中超氧化物歧化酶活性以及铜锌超氧化物歧化酶和谷胱甘肽过氧化物酶的mRNA表达,同时降低了GSH/GSSG比值,提高了丙二醛水平。DEX处理加重了肝脏的氧化损伤,因此增加了肉鸡对腹水综合征的敏感性,导致更高的死亡率并降低了生长性能。血清代谢组学分析表明,DEX处理显著提高了葡萄糖、蛋白质代谢中间产物(缬氨酸、脯氨酸、丝氨酸、苏氨酸和尿素)以及脂质代谢相关产物(棕榈酸酯、硬脂酸和胆固醇)的水平,同时降低了β-羟基丁酸、琥珀酸和苹果酸的水平,表明DEX处理抑制了肉鸡肝脏中的三羧酸循环和脂肪酸氧化,并促进了脂肪酸的从头合成以及蛋白质分解。此外,对代谢相关酶的检测表明,DEX处理抑制了糖酵解并促进了糖原分解。总之,DEX处理导致了肉鸡的氧化应激以及葡萄糖和脂质代谢紊乱。

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