The Effects of In Ovo Feeding of Selenized Glucose on Selenium Concentration and Antioxidant Capacity of Breast Muscle in Neonatal Broilers.

This study aims to investigate the impacts of in ovo feeding (IOF) of selenized glucose (SeGlu) on selenium (Se) level and antioxidant capacity of breast muscle in newborn broilers. After candling on 16 day of incubation, a total of 450 eggs were randomly divided into three treatments. On the 17.5th day of incubation, eggs in a control treatment were injected with 0.1 mL of physiological saline (0.75%), while the 2nd group and 3rd group were supplied with 0.1 mL of physiological saline containing 10 µg Se from SeGlu (SeGlu10 group) and 20 µg Se from SeGlu (SeGlu20 group). The results showed that in ovo injection in both SeGlu10 and SeGlu20 increased the Se level and reduced glutathione concentration (GSH) in pectoral muscle of hatchlings (P < 0.05). Compared with the control group, the SeGlu20-treated chicks significantly enhanced the activity of the superoxide dismutase (SOD) and mRNA expression of NAD(P)H quinone dehydrogenase 1 (NQO1) in breast muscle, while there was upregulation in mRNA expressions of glutathione peroxidase 1 (GPX-1) and thioredoxin reductase 1 (TrxR1) and higher total antioxidant capacity (T-AOC) in SeGlu10 treatment (P < 0.05). However, no significant difference on enzyme activities of glutathione peroxidase (GR), glutathione reductase, thioredoxin reductase, concentration of malondialdehyde, and free radical scavenging ability (FRSA) of superoxide radical (O2-•) and hydroxyl radical (OH•) was observed among the three treatments (P > 0.05). Therefore, IOF of SeGlu enhanced Se deposition in breast muscle of neonatal broilers. In addition, in ovo injection of SeGlu could increase the antioxidant capacity of newborn chicks possibly through upregulating the mRNA expression of GPX1, TrxR1, and NQO1, as well as the SOD activity.

Supplementing cholamine to diet lowers laying rate by promoting liver fat deposition and altering intestinal microflora in laying hens.

The effects of cholamine, a raw material for synthesis of some active lipids, are unknown in poultry. To address this, 180 52-wk-old Hyline laying hens were randomly divided into 3 groups (20 replicates per group with three hens per replicate). The control group and the treatment groups (treatment 1 and 2) were fed basal diet and the diet supplemented with 500 or 1,000 mg of cholamine per kilogram of the diet for 35 d, respectively. The data showed that supplementary cholamine significantly lowered egg production, daily feed intake, serum high-density lipoprotein cholesterol level, liver index, and the percentages of C15:0 and C20:0 in fatty acid composition of liver, significantly elevated hepatic triglyceride content, the ratio of villus height to crypt depth (P < 0.05), and the percentage of C18:2n-6 and the ratio of n-6 to n-3 polyunsaturated fatty acids in liver fat (P < 0.10). Moreover, supplementary cholamine altered the relative abundance of some intestinal bacteria with a decrease in the alpha biodiversity (P < 0.10). Additionally, transcriptome analysis on the livers of the treatment vs. the control groups identified 1,151 up- and 914 down-regulated differentially expressed genes (DEGs), and pathway analysis revealed that the suppressed Notch signaling pathway and the enhanced Oxidative phosphorylation pathway were enriched with DEGs. Particularly, fat absorption, transport and oxidative phosphorylation-related DEGs (e.g., FABP1, APOA4, and PCK1) were significantly induced, but fatty acid synthesis, and lipid package and secretion-related DEGs (e.g., FASN, SCD, and MTTP) were not. In conclusion, supplementary cholamine may lower egg production by promoting hepatic lipid deposition and reducing abundances of beneficial intestinal bacteria and microfloral biodiversity in laying hens.

Dietary Selenized Glucose Increases Selenium Concentration and Antioxidant Capacity of the Liver, Oviduct, and Spleen in Laying Hens.

Selenized glucose (SeGlu) is a new type of organic selenium (Se) that is synthesized through the selenide reaction of glucose with sodium hydrogen selenide. This study aimed to clarify the influence of dietary SeGlu on the Se level and antioxidant capacity of the liver, oviduct, and spleen in laying hens. A total of 360, 60-week-old, Hy-Line Brown laying hens were randomly assigned to three treatment groups: a basal diet alone (control group, without adding exogenous Se) or the basal diet supplemented with 0.3 mg/kg of Se from sodium selenite (SS) or 5 mg/kg of Se from SeGlu. Diets with SeGlu increased Se levels in the liver, oviduct, and spleen of laying hens (P < 0.001). Compared with the control and SS groups, diet supplemented with SeGlu enhanced glutathione peroxidase (GSH-Px) activity and total antioxidant capacity (T-AOC) in the spleen and oviduct as well as the scavenging ability of 2, 2-diphenyl-1-picrylhydrazyl free radical (DPPH•) in the oviduct (P < 0.05). Compared with the control group, SeGlu treatment resulted in an increase (P < 0.05) in GSH-Px activity, T-AOC, and scavenging abilities of hydroxyl radical and DPPH• in the liver of hens. In addition, dietary SeGlu and SS decreased the hydrogen peroxide level in the oviduct in comparison to the control group (P < 0.05). Therefore, dietary SeGlu increased Se concentration and antioxidant ability in the liver, oviduct, and spleen of laying hens. Moreover, SeGlu may be used as a potential source of Se additive in laying hen production.

Analysis of gene expression and regulation implicates C2H9orf152 has an important role in calcium metabolism and chicken reproduction.

The reproductive system of a female bird is responsible for egg production. The genes highly expressed in oviduct are potentially important. From RNA-seq analysis, C2H9orf152 (an orthologous gene of human C9orf152) was identified as highly expressed in chicken uterus. To infer its function, we obtained and characterized its complete cDNA sequence, determined its spatiotemporal expression, and probed its transcription factor(s) through pharmaceutical approach. Data showed that the complete cDNA sequence was 1468bp long with a 789bp of open reading frame. Compared to other tested tissues, this gene was highly expressed in the oviduct and liver tissues, especially uterus. Its expression in uterus was gradually increased during developmental and reproductive periods, which verified its involvement in the growth and maturity of reproductive system. In contrast, its expression was not significant different between active and quiescent uterus, suggesting the role of C2H9orf152 in reproduction is likely due to its long-term effect. Moreover, based on its 5'-flanking sequence, Foxd3 and Hnf4a were predicted as transcription factors of C2H9orf152. Using berberine or retinoic acid (which can regulate the activities of Hnf4a and Foxd3, respectively), we demonstrated suppression of C2H9orf152 by the chemicals in chicken primary hepatocytes. As retinoic acid regulates calcium metabolism, and Hnf4a is a key nuclear factor to liver, these findings suggest that C2H9orf152 is involved in liver function and calcium metabolism of reproductive system. In conclusion, C2H9orf152 may have a long-term effect on chicken reproductive system by regulating calcium metabolism, suggesting this gene has an important implication in the improvement of egg production and eggshell quality.

Supplementing dietary sugar promotes endoplasmic reticulum stress-independent insulin resistance and fatty liver in goose.

It is known that endoplasmic reticulum stress (ERS) contributes to insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) in mammals. However, we recently demonstrated that overfeeding with a traditional diet (mainly consisting of cooked maize) does not induce ERS in goose. As cellular studies show that high glucose and palmitate can trigger ERS in mammalian cells, we hypothesized that supplementing sugar to the traditional diet could induce ERS, thus promoting insulin resistance and fatty liver. To test the hypothesis, we first treated goose primary hepatocytes with high glucose (25 mM and 50 mM) and palmitate (0.5 mM) supplemented with or without 0.25 mM oleate. Data indicated that, as in mammalian cells, high glucose and palmitate indeed induced ERS in goose primary hepatocytes, and palmitate-induced ERS was suppressed by supplemental 0.25 mM oleate. We then tested the hypothesis with an in vivo study, in which Landes geese overfed with traditional or novel diets (i.e., the traditional diet supplemented with sugar) were compared with control geese (normally fed with cooked maize) for ERS, IR and fatty liver. The differences in glucose tolerance, insulin tolerance and postprandial blood glucose between the geese overfed with traditional and novel diets suggested that supplementing dietary sugar promoted IR. This promotion was accompanied with an increasing trend of liver weight and abdominal fat weight relative to body weight. Surprisingly, compared to overfeeding with the traditional diet, overfeeding with the novel diet did not induce ERS, even further suppressed ERS in goose fatty liver. Together, our findings suggest that supplementing dietary sugar promotes ERS-independent IR and fatty liver in goose. It is intriguing to discover the factor(s) protecting goose liver from ERS as well as the non-ERS mechanism underlying IR.

Prosteatotic genes are associated with unsaturated fat suppression of saturated fat-induced hepatic steatosis in C57BL/6 mice.

Both high sugar and fat diets can induce prosteatotic genes, leading to obesity and obesity-associated diseases, including hepatic steatosis. Unsaturated fat/fatty acid (USFA) reduces high sugar-induced hepatic steatosis by inhibiting the induced prosteatotic genes. In contrast, it is still unclear how USFA ameliorates saturated fat/fatty acid (SFA)-induced hepatic steatosis. As sugar and fat have different transport and metabolic pathways, we hypothesized that USFA suppressed SFA-induced hepatic steatosis via a different set of prosteatotic genes. To test this, we implemented high SFA vs USFA diets and a control diet in C57BL/6 mice for 16 weeks. Severe hepatic steatosis was induced in mice fed the SFA diet. Among a nearly complete set of prosteatotic genes, only the stearoyl-coenzyme a desaturase 1 (Scd1), cluster of differentiation 36 (Cd36), and peroxisome proliferator-activated receptor γ (Pparγ) genes that were differentially expressed in the liver could contribute to SFA-induced steatosis or the alleviative effect of USFA. That is, the SFA diet induced the expression of Cd36 and Pparγ but not Scd1, and the USFA diet suppressed Scd1 expression and the induction of Cd36 and Pparγ. These findings were mainly recapitulated in cultured hepatocytes. The essential roles of SCD1 and CD36 were confirmed by the observation that the suppression of SCD1 and CD36 with small interfering RNA or drug treatment ameliorated SFA-induced lipid accumulation in hepatocytes. We thus concluded that SCD1, CD36, and PPARγ were essential to the suppression of SFA-induced hepatic steatosis by main dietary USFA, which may provide different therapeutic targets for reducing high-fat vs sugar-induced hepatic steatosis.