Xu Jingyang, Wang Longqiong, Tang Jiayong, Jia Gang, Liu Guangmang, Chen Xiaoling, Cai Jingyi, Shang Haiying, Zhao Hua
Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, Sichuan, China.
Trace Element Research Center, Sichuan Agricultural University, Chengdu, Sichuan, China.
PLoS One. 2017 Aug 1;12(8):e0182079. doi: 10.1371/journal.pone.0182079. eCollection 2017.
This study was envisaged to comprehensively profile genes in selected tissues along with a few biochemical indicators and integrate resulting information with dietary selenium (Se) deficiency symptoms in broilers. A total of 120 one-day-old Cobb male broilers were equally divided into two groups and fed a Se deficient corn-soybean-based basal diet supplemented with 0.3 mg/kg sodium selenite (Control, Se adequate) or without selenite (Se deficiency) for five weeks. Effects of Se deficiency on mRNA abundance of twenty-three selenoprotein encoding genes and seventeen insulin signaling related genes were studied at day 35 in pancreas, liver and muscle along with plasma biochemical constituents and enzyme activities. Compared to healthy birds in control diet, Se deficient diet induced deficiency symptoms in 90% birds and classic nutritional pancreatic atrophy, depressed growth performance of broilers, and decreased (P < 0.01 to P < 0.05) total antioxidant capacity and activities of superoxide dismutase and glutathione peroxidase in plasma and three other tissues. Se deficiency resulted in 58% higher mortality than control birds. Dietary Se deficiency down-regulated (P < 0.01-0.05) eighteen selenoprotein encoding genes in pancreas, fourteen genes in muscle and nine genes in liver, and up-regulated (P < 0.05) Txnrd1 and Selx in liver. Meanwhile, six, thirteen and five insulin signaling related genes were down-regulated (P < 0.01-0.05) in pancreas, muscle and liver, respectively, and three genes were up-regulated (P < 0.01) in liver. The decrease (P < 0.05) in levels of plasma insulin, total triglyceride and total cholesterol, and concurrent elevated (P < 0.05) levels of plasma glucose and inflammatory cytokines accompanied the global down-regulation of selenoprotein encoding- and insulin signaling related- genes in Se deficient birds. It was concluded that dietary Se deficiency induces nutritional pancreatic atrophy and metabolic disorder of glucose and lipid in broilers via down-regulation of selenoprotein encoding- and insulin signaling related- genes, indicating potential roles of these genes in metabolic regulation.
本研究旨在全面分析选定组织中的基因以及一些生化指标,并将所得信息与肉鸡的膳食硒(Se)缺乏症状相结合。总共120只1日龄的科宝雄性肉鸡被平均分为两组,分别饲喂添加0.3 mg/kg亚硒酸钠的缺硒玉米-大豆基础日粮(对照组,硒充足)或不添加亚硒酸钠的日粮(缺硒组),持续五周。在第35天,研究了缺硒对胰腺、肝脏和肌肉中23个硒蛋白编码基因和17个胰岛素信号相关基因的mRNA丰度的影响,同时还研究了血浆生化成分和酶活性。与对照日粮组的健康鸡相比,缺硒日粮使90%的鸡出现缺乏症状和典型的营养性胰腺萎缩,降低了肉鸡的生长性能,并使血浆和其他三个组织中的总抗氧化能力以及超氧化物歧化酶和谷胱甘肽过氧化物酶的活性降低(P<0.01至P<0.05)。缺硒导致的死亡率比对照鸡高58%。膳食缺硒使胰腺中18个硒蛋白编码基因、肌肉中14个基因和肝脏中9个基因表达下调(P<0.01-0.05),并使肝脏中的Txnrd1和Selx表达上调(P<0.05)。同时,胰腺、肌肉和肝脏中分别有6个、13个和5个胰岛素信号相关基因表达下调(P<0.01-0.05),肝脏中有3个基因表达上调(P<0.01)。缺硒鸡中硒蛋白编码基因和胰岛素信号相关基因的整体下调伴随着血浆胰岛素、总甘油三酯和总胆固醇水平的降低(P<0.05),以及血浆葡萄糖和炎性细胞因子水平的同时升高(P<0.05)。得出的结论是,膳食缺硒通过下调硒蛋白编码基因和胰岛素信号相关基因,诱导肉鸡出现营养性胰腺萎缩以及葡萄糖和脂质代谢紊乱,表明这些基因在代谢调节中具有潜在作用。