Abstract
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.
Highlights
Selenium (Se) is an essential micronutrient in animals and human that has been shown to exert its important biological functions through selenoproteins [1, 2]
Birds of Se deficient group displayed classic Se deficiency clinical symptoms characterized by edema or cyanotic patches in ventral parts of body such as breast, under the wings, ventral surface of the face, down the legs, abdomen and mandibular space
We found that the Se deficient diet globally down-regulated thirteen insulin signaling related genes (Akt1, Braf, forkhead box O 1 (Foxo1), forkhead box A2 (Foxa2), insulin receptor (Ir), Irs1, Irs2, Ins, neurogenic differentiation 1 (Neurod1), Ptpn1, phosphoinositide 3-kinase (Pi3k), Slc2A2, and Ucp) in muscle (Fig 5B)
Summary
Selenium (Se) is an essential micronutrient in animals and human that has been shown to exert its important biological functions through selenoproteins [1, 2]. Selenate shows regulatory effects on glycolytic, gluconeogenic and fatty acid metabolism pathways which are disturbed in diabetic disorders [15] and sodium selenite stimulates glucose uptake in cultivated adipocytes and dissected skeletal muscle of rats [16, 17]. Both insulin signaling and insulin secretion are linked to the cellular redox state [18,19,20], providing a rationale for an interference of Se and antioxidant selenoproteins with insulin regulated metabolic pathways. Se deficiency results in exudative diathesis, pancreatic atrophy [4] and changes of histomorphology and cell structure of pancreas [21] in chicken, which indicates that Se is a key factor to ensure normal functioning of the pancreas, as well the synthesis and function of insulin
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