We previously determined the effects of dietary selenium (Se) deficiency or excess on mRNA abundance of 12 selenoprotein genes in pig tissues. In this study, we determined the effect of dietary Se on mRNA levels of the remaining porcine selenoprotein genes along with protein production of 4 selenoproteins (Gpx1, Sepp1, Selh, and Sels) and body glucose homeostasis. Weanling male pigs (n = 24) were fed a Se-deficient (<0.02 mg Se/kg), basal diet supplemented with 0, 0.3, or 3.0 mg Se/kg as Se-enriched yeast (Angel Yeast) for 16 wk. Although mRNA abundance of the 13 selenoproteins in 10 tissues responded to dietary Se in 3 patterns, there was no common regulation for any given gene across all tissues or for any given tissue across all genes. Dietary Se affected (P < 0.05) 2, 3, 3, 5, 6, 7, 7, and 8 selenoprotein genes in muscle, hypothalamus, liver, kidney, heart, spleen, thyroid, and pituitary, respectively. Protein abundance of Gpx1, Sepp1, Selh, and Sels in 6 tissues was regulated (P < 0.05) by dietary Se concentrations in 3 ways. Compared with those fed 0.3 mg Se/kg, pigs fed 3.0 mg Se/kg became hyperinsulinemic (P < 0.05) and had lower (P < 0.05) tissue levels of serine/threonine protein kinase. In conclusion, dietary Se exerted no global regulation of gene transcripts or protein levels of individual selenoproteins across porcine tissues. Pigs may be a good model for studying mechanisms related to the potential prodiabetic risk of high-Se intake in humans.

Although supranutrition of selenium (Se) is considered a promising anti-cancer strategy, recent human studies have shown an intriguing association between high body Se status and diabetic risk. This study was done to determine if a prolonged high intake of dietary Se actually induced gestational diabetes in rat dams and insulin resistance in their offspring. Forty-five 67-day-old female Wistar rats (n=15/diet) were fed a Se-deficient (0.01 mg/kg) corn–soy basal diet (BD) or BD+Se (as Se-yeast) at 0.3 or 3.0 mg/kg from 5 weeks before breeding to day 14 postpartum. Offspring (n=8/diet) of the 0.3 and 3.0 mg Se/kg dams were fed with the same respective diet until age 112 days. Compared with the 0.3 mg Se/kg diet, the 3.0 mg/kg diet induced hyperinsulinemia (P<0.01), insulin resistance (P<0.01), and glucose intolerance (P<0.01) in the dams at late gestation and/or day 14 postpartum and in the offspring at age 112 days. These impairments concurred with decreased (P<0.05) mRNA and/or protein levels of six insulin signal proteins in liver and muscle of dams and/or pups. Dietary Se produced dose-dependent increases in Gpx1 mRNA or GPX1 activity in pancreas, liver, and erythrocytes of dams. The 3.0 mg Se/kg diet decreased Selh (P<0.01), Sepp1 (P=0.06), and Sepw1 (P<0.01), but increased Sels (P<0.05) mRNA levels in the liver of the offspring, compared with the 0.3 mg Se/kg diet. In conclusion, supranutrition of Se as a Se-enriched yeast in rats induced gestational diabetes and insulin resistance. Expression of six selenoprotein genes, in particular Gpx1, was linked to this metabolic disorder.

This study aims to investigate the effect of zearalenone supplementation on rat metabolism. Rats received biweekly intragastric administration of zearalenone mycotoxin (3 mg/kg body weight) for 2 weeks. Urine and plasma samples after zearalenone administration were analyzed by NMR-based metabolomics. Zearalenone exposure significantly elevated the plasma levels of glucose, lactate, N-acetyl glycoprotein, O-acetyl glycoprotein, and propionate but reduced the plasma levels of tyrosine, branched-chain amino acids, and choline metabolites. Zearalenone supplementation decreased the urine levels of butyrate, lactate, and nicotinate. However, it increased the urine levels of allantoin, choline, and N-methylnicotinamide at 0-8 h after the last zearalenone administration and those of 1-methylhistidine, acetoacetate, acetone, and indoxyl sulfate at 8-24 h after the last zearalenone administration. These results suggest that zearalenone exposure can cause oxidative stress and change common systemic metabolic processes, including cell membrane metabolism, protein biosynthesis, glycolysis, and gut microbiota metabolism.

We demonstrate a novel all-fiber-optic humidity sensor comprised of a WS₂ film overlay on a side polished fiber (SPF). This sensor can achieve optical power variation of up to 6 dB in a relative humidity (RH) range of 35%-85%. In particular, this novel humidity fiber sensor has a linear correlation coefficient of 99.39%, sensitivity of 0.1213 dB/%RH, and a humidity resolution of 0.475%RH. Furthermore, this sensor shows good repeatability and reversibility, and fast response to breath stimulus. This WS₂ based all-fiber optic humidity sensor is easy to fabricate, is compatible with pre-established fiber optic systems, and holds great potential in photonics applications such as in all-fiber optic humidity sensing networks.

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.

The high-fat diet induced inflammation in pigs and affected their gene expression of selenoproteins associated with thioredoxin and oxidoreductase systems, local tissue thyroid hormone activity, endoplasmic reticulum protein degradation, and phosphorylation of lipids. This porcine model may be used to study interactive mechanisms between excess fat intake and selenoprotein function.

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The objective of this study was to determine the effects of increased AA and energy intake during late gestation on reproductive performance, milk composition, and metabolic and redox status of sows. A total of 118 Yorkshire sows (third through sixth parity) were randomly assigned to dietary treatments from day 90 of gestation until farrowing. Dietary treatments consisted of combinations of 2 standardized ileal digestible (SID) AA levels [14.7 or 20.6 g/d SID Lys, SID Lys and other AA met or exceeded the NRC (2012) recommendations] and 2 energy levels (28.24 or 33.78 MJ/d intake of NE) in a 2 × 2 factorial design. After parturition, all sows were fed a standard lactation diet. Blood samples were collected and analyzed for parameters on metabolism, redox status, and amino acid profile. The data were analyzed using the generalized linear mixed models to reveal the impact of dietary levels of energy, AA, and their interaction. Sows with increased intake of AA had greater BW gain (P < 0.01) during late gestation. Furthermore, the BW loss during lactation was increased in sows with increasing intake of energy (P < 0.05) or AA (P < 0.05). Sows fed high energy had higher total litter birth weights (20.2 kg vs. 18.4 kg, P < 0.05) and shorter duration of farrowing (261 min vs. 215 min, P < 0.05), compared with those fed low energy, which likely was due to higher (P < 0.05) plasma glucose and lower (P < 0.05) plasma lactate prior to parturition. High AA intake in late gestation increased the ADG of piglets during the following lactation (P < 0.05), and increased the concentrations of plasma urea, and the following AA: Lys, Met, Thr, Val, Ile, Leu, Phe, Asp, Ser, and Arg at farrowing (P < 0.05). In conclusion, the increased intake of energy increased total litter weight of newborns and shortened the farrowing duration, which likely was due to improved energy status at farrowing. Furthermore, sows with increased intake of AA led to higher growth rate of piglets during the following lactation, accompanying with the increasing levels of plasma urea and amino acids. Therefore, the higher energy intake in late gestation appeared to improve litter weight and farrowing duration, while higher AA intake may have positive effect on piglets performance in lactation.