We previously determined the effects of dietary selenium (Se) deficiency or excess on mRNA abundance of 12 selenoprotein genes in pig tissues. In thi

With the increasing of global mean surface air temperature, heat stress (HS) induced by extreme high temperature has become a key factor restricting the poultry industry. Liver is the main metabolic organ of broilers, HS induces liver damage and metabolic disorders, which impairs the health of broilers and affects food safety. As an essential trace element for animals, selenium (Se) involves in the formation of antioxidant system, and its biological functions are generally mediated by selenoproteins. However, the mechanism of Se against HS induced liver damage and metabolic disorders in broilers is inadequate. Therefore, we developed the chronic heat stress (CHS) broiler model and investigated the potential protection mechanism of organic Se (selenomethionine, SeMet) on CHS induced liver damage and metabolic disorders. In present study, CHS caused liver oxidative damage, and induced hepatic lipid accumulation and glycogen infiltration of broilers, which are accompanied by mitochondrial dysfunction, abnormal mitochondrial tricarboxylic acid (TCA) cycle and endoplasmic reticulum (ER) stress. Dietary SeMet supplementation increased the hepatic Se concentration and exhibited protective effects via promoting the expression of selenotranscriptome and several key selenoproteins (GPX4, TXNRD2, SELENOK, SELENOM, SELENOS, SELENOT, GPX1, DIO1, SELENOH, SELENOU and SELENOW). These key selenoproteins synergistically improved the antioxidant capacity, and mitigated the mitochondrial dysfunction, abnormal mitochondrial TCA cycle and ER stress, thus recovered the hepatic triglyceride and glycogen concentration. What's more, SeMet supplementation suppressed lipid and glycogen biosynthesis and promoted lipid and glycogen breakdown in liver of broilers exposed to CHS though regulating the AMPK signals. Overall, our present study reveals a potential mechanism that Se alleviates environment HS induced liver damage and glycogen and lipid metabolism disorders in broilers, which provides a preventive and/or treatment measure for environment HS-dependent hepatic metabolic disorders in poultry industry.

Background: Relations of the 25 mammalian selenoprotein genes with obesity and the associated inflammation remain unclear.Objective: This study explor

The aim of this study was to investigate the effect of naringin on lipopolysaccharide (LPS)-induced jejunal barrier function in mice. Forty-five 3-week-old healthy male Balb/c mice with similar body weights were randomly divided into control group, LPS group, LPS + naringin group, with 15 mice in each treatment group. The mice were intraperitoneally injected with the same dose of saline or LPS (10 mg per kg BW) at 43 d. The blood samples, liver and jejunal tissues were collected after 3 h of injection. The results showed that LPS significantly increased the serum diamine oxidase (DAO) activity, D-lactate (D-LA) concentration, and malondialdehyde (MDA) content in liver and jejunum, while decreased the activities of superoxide dismutase (SOD), glutathione peroxidase (Gpx) and catalase (CAT) in liver and jejunum. The LPS treatment caused an increase in the crypt depth and a decrease in the villus height and the ratio of villus height to crypt depth (V/C) of the jejunum. In addition, the LPS treatment significantly increased the mRNA expressions of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, toll-like receptor 4 (TLR4), p38-mitogen-activated protein kinase (p38 MAPK), nuclear factor-κB (NF-κB) and kelch-like ECH-associated protein 1 (Keap1), while decreased mRNA expressions of zonula occludens 1 (ZO-1), occludin, claudin, mucin 2 (MUC2) and junctional adhesion molecule 2 (JAM2), Gpx, SOD1, GST, CAT and nuclear factor-erythroid 2-related factor 2 (Nrf2). However, the naringin treatment mitigated these effects induced by LPS. Taken together, our findings suggested that naringin attenuates LPS-induced intestinal barrier damage by inhibiting inflammatory factors and improving antioxidant function and intestinal tight junction, which might be mediated by activating the Nrf2 signaling and suppressing the TLR4/p38 MAPK/NF-κB signaling.

The present study compared the protective effect of sodium selenite (SS) and selenomethionine (SeMet) on heat stress (HS)-invoked porcine IPEC-J2 cellular damage and integrate potential roles of corresponding selenoprotein. Cells were cultured at 37°C until 80 % confluence and then subjected to four different conditions for 24 h: at 37°C (control), 41·5°C (HS), 41·5°C supplied with 0·42 µmol Se/L SS (SS), or SeMet (SeMet). HS significantly decreased cell viability, up-regulated mRNA and protein levels of heat shock protein 70 (HSP70) and down-regulated mRNA and protein levels of tight junction-related proteins (claudin-1 (CLDN-1) and zonula occludens-1 (ZO-1)). HS-induced cell injury was associated with the up-regulation (P < 0·05) of six inflammation-related genes and fourteen selenoprotein encoding genes and down-regulation (P < 0·05) of two inflammation-related genes and five selenoprotein encoding genes. Compared with the HS group, SS and SeMet supplementation resulted in an increase (P < 0·05) in cell viability, decreased (P < 0·05) mRNA expression of HSP70 and six inflammation-related genes and rescue (P < 0·05) of mRNA and protein levels of CLDN-1 and ZO-1. SS and SeMet supplementation changes the expressions of nineteen selenoprotein encoding genes in cells affected by HS. Both Se supplementation significantly recovered the protein level of glutathione peroxidase-1 and increased selenoprotein P in the IPEC-J2 cells under HS, respectively. In summary, Se supplementation alleviated the negative impact of HS on IPEC-J2 cells, and their cellular protective effect was associated with regulation expression of selenoproteins, and SeMet exhibited a better protective effect.

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.