Effects of carriers for oils in compound feeds on growth performance, nutrient digestibility, and gut microbiota in broiler chickens.

Carrier materials for oils in compound feeds may be used in animal nutrition to supply liquid feed additives. However, implications of such carriers for the digestibility of the contained oil are unknown. This study investigated the potential of oil carriers in compound feed and their effect on performance, metabolizable energy, fatty acid (FA) retention, amino acid (AA) digestibility, and gut microbiota in broiler chickens. Six experimental diets were formulated following a 2 × 3 factorial arrangement with 20 g/kg or 40 g/kg of rapeseed oil supplied with no carrier or bound in a silica-based (SC) or lignocellulose-based (LC) carrier in a 1:1 mass ratio. The diets were assigned to 48 metabolism units with 15 animals each based on a randomized complete block design and fed from d 18 to 28 of the trial. Total excreta were collected from d 24 to 27 and used to determine total tract retention (TTR) of FA and MEn. On d 28, AA digestibility both by the distal half of the jejunum and the distal half of the ileum was determined, and microbiota of ileal and cecal digesta was analyzed using 16S ribosomal RNA sequencing. There were significant interactions for ADG, ADFI, the gain:feed ratio (G:F), MEn, and the TTR of crude fat and most fatty acids (P ≤ 0.046) except for C18, C18:2, and C22:0. Addition of SC decreased ADG, ADFI, and G:F (P < 0.001), while LC at 40 g/kg oil inclusion increased G:F and MEn (P < 0.001) for both inclusion levels. The TTR of crude fat and the FA C18:1, C18:2, C18:3, and C22:0 was increased by the addition of SC (P ≤ 0.016), while LC increased the TTR of the FA C18:1 and C18:2 as well as the TTR of C18:3 at 20 g/kg oil inclusion (P ≤ 0.016). Adding SC and LC increased the digestibility of 7 and 2 AA by the distal half of the jejunum, respectively, and the digestibility of 8 and 13 AA by the distal half of the ileum, respectively (P ≤ 0.039). The ß-diversity and abundance of some taxa were altered by addition of LC and SC in the ceca while no treatment effect on the ileal microbiota was found. The results give no indication of an incomplete release of the oil from the carriers because the TTR of most FA was increased upon addition of SC and LC. LC may be used to supply liposoluble feed additives without drawbacks for nutrient digestibility and growth while SC requires further examination.

Impact of selenite and selenate on differentially expressed genes in rat liver examined by microarray analysis.

Sodium selenite and sodium selenate are approved inorganic Se (selenium) compounds in human and animal nutrition serving as precursors for selenoprotein synthesis. In recent years, numerous additional biological effects over and above their functions in selenoproteins have been reported. For greater insight into these effects, our present study examined the influence of selenite and selenate on the differential expression of genes encoding non-selenoproteins in the rat liver using microarray technology. Five groups of nine growing male rats were fed with an Se-deficient diet or diets supplemented with 0.20 or 1.0 mg of Se/kg as sodium selenite or sodium selenate for 8 weeks. Genes that were more than 2.5-fold up- or down-regulated by selenite or selenate compared with Se deficiency were selected. GPx1 (glutathione peroxidase 1) was up-regulated 5.5-fold by both Se compounds, whereas GPx4 was up-regulated by only 1.4-fold. Selenite and selenate down-regulated three phase II enzymes. Despite the regulation of many other genes in an analogous manner, frequently only selenate changed the expression of these genes significantly. In particular, genes involved in the regulation of the cell cycle, apoptosis, intermediary metabolism and those involved in Se-deficiency disorders were more strongly influenced by selenate. The comparison of selenite- and selenate-regulated genes revealed that selenate may have additional functions in the protection of the liver, and that it may be more active in metabolic regulation. In our opinion the more pronounced influence of selenate compared with selenite on differential gene expression results from fundamental differences in the metabolism of these two Se compounds.

Regulation of the insulin antagonistic protein tyrosine phosphatase 1B by dietary Se studied in growing rats.

Protein tyrosine phosphatase 1B (PTP1B) is a key enzyme in the counterregulation of insulin signaling, and its physiological modulation depends on H2O2 and glutathione (GSH). Se via GSH peroxidases (GPxs) and its specific metabolism is involved in the removal of H2O2 and in the regulation of GSH metabolism. Recent results from animal trials and epidemiological studies with humans have shown that a high GPx1 activity or a permanent surplus of Se may promote the development of obesity and diabetes. Our nutrition physiological study with 7 x 7 growing rats was carried out to examine if PTP1B is modulated by Se supplements and, thus, may represent one trigger mediating these undesirable metabolic effects of Se. One group of rats was fed an Se-deficient diet for 8 weeks. The diets of the other six groups contained Se as selenite or selenate according to the recommendations (0.20 mg/kg diet) and at two supranutritional levels (1.00 and 2.00 mg/kg diet). All Se-supplemented animals featured a significantly higher body weight (6-14%) compared to their Se-deficient companions. Expression and activity of GPx1 in the liver of Se supplemented animals was 10- and 70-fold higher compared to Se deficiency. The detailed study of PTP1B regulation using an enzymatic assay and Western Blot analysis with an antibody against protein glutathionylation revealed that PTP1B was significantly up-regulated by both a maximization of GPx1 activity and by increasing dietary Se supply, reducing its inhibition via glutathionylation. Selenate effected a stronger PTP activation compared to selenite. In conclusion, our results suggest that the modulation of PTP1B activity may represent one plausible mechanism by which a long-term intake of Se supplements exceeding the requirements can promote the development of obesity and diabetes and needs further intensive investigation.

Effect of selenium deficiency on the antioxidative status and muscle damage in growing turkeys.

An experiment investigated the effect of different selenium supplementations on the antioxidant defence system and on the occurrence of muscle dystrophy in growing turkeys. Newly hatched male turkeys (B.U.T. Big 6) were divided into eight groups of 18 turkeys each and fed either a basal diet (selenium < 0.010 mg/kg diet), or the basal diet supplemented with 0.10; 0.15; 0.20; 0.25; 0.30; 0.35 or 0.40 mg selenium/kg diet in the form of sodium selenate. Vitamin E was adequately supplemented in all diets. After 35 days, muscle damage parameters including aspartate aminotransferase, creatine kinase, creatine kinase M and B were significantly increased in the selenium deficient Group I. A significant reduction of weight gain, feed consumption and selenium dependent glutathione peroxidase activity was also observed in the liver of selenium deficient birds. The ratio of oxidised glutathione (GSSG) to total glutathione (tGSH) was substantially altered in the selenium deficient Group I as well as in Group II (0.10 mg selenium/kg feed). The activity of glutathione reductase (GR) and glutathione-S-transferase (GST) was not affected by selenium deficiency.