No abstract

Poultry in commercial settings are exposed to a range of stressors. A growing body of information clearly indicates that excess ROS/RNS production and oxidative stress are major detrimental consequences of the most common commercial stressors in poultry production. During evolution, antioxidant defence systems were developed in poultry to survive in an oxygenated atmosphere. They include a complex network of internally synthesised (e.g., antioxidant enzymes, (glutathione) GSH, (coenzyme Q) CoQ) and externally supplied (vitamin E, carotenoids, etc.) antioxidants. In fact, all antioxidants in the body work cooperatively as a team to maintain optimal redox balance in the cell/body. This balance is a key element in providing the necessary conditions for cell signalling, a vital process for regulation of the expression of various genes, stress adaptation and homeostasis maintenance in the body. Since ROS/RNS are considered to be important signalling molecules, their concentration is strictly regulated by the antioxidant defence network in conjunction with various transcription factors and vitagenes. In fact, activation of vitagenes via such transcription factors as Nrf2 leads to an additional synthesis of an array of protective molecules which can deal with increased ROS/RNS production. Therefore, it is a challenging task to develop a system of optimal antioxidant supplementation to help growing/productive birds maintain effective antioxidant defences and redox balance in the body. On the one hand, antioxidants, such as vitamin E, or minerals (e.g., Se, Mn, Cu and Zn) are a compulsory part of the commercial pre-mixes for poultry, and, in most cases, are adequate to meet the physiological requirements in these elements. On the other hand, due to the aforementioned commercially relevant stressors, there is a need for additional support for the antioxidant system in poultry. This new direction in improving antioxidant defences for poultry in stress conditions is related to an opportunity to activate a range of vitagenes (via Nrf2-related mechanisms: superoxide dismutase, SOD; heme oxygenase-1, HO-1; GSH and thioredoxin, or other mechanisms: Heat shock protein (HSP)/heat shock factor (HSP), sirtuins, etc.) to maximise internal AO protection and redox balance maintenance. Therefore, the development of vitagene-regulating nutritional supplements is on the agenda of many commercial companies worldwide.

No abstract

The apparent DE and ME values of crude glycerol for growing pigs were determined in 5 experiments using crude glycerol (86.95% glycerol) from a biodiesel production facility, which used soybean oil as the initial feedstock. Dietary treatments were 0, 5, or 10% glycerol addition to basal diets in Exp. 1; 0, 5, 10, or 20% glycerol addition to basal diets in Exp. 2; and 0 and 10% crude glycerol addition to the basal diets in Exp. 3, 4, and 5. Each diet was fed twice daily to pigs in individual metabolism crates. After a 10-d adjustment period, a 5-d balance trial was conducted. During the collection period, feces and urine were collected separately after each meal and stored at 0 degrees C until analyses. The GE of each dietary treatment and samples of urine and feces from each pig were determined by isoperibol bomb calorimetry. Digestible energy of the diet was calculated by subtracting fecal energy from the GE in the feed, whereas ME was calculated by subtracting the urinary energy from DE. The DE and ME values of crude glycerol were estimated as the slope of the linear relationship between either DE or ME intake from the experimental diet and feed intake. Among all experiments, the crude glycerol (86.95% glycerol) examined in this study was shown to have a DE of 3,344 +/- 8 kcal/kg and an ME of 3,207 +/- 10 kcal/kg, thereby providing a highly available energy source for growing pigs.

Three energy balance experiments were conducted to determine AMEn of glycerin using broiler chickens of diverse ages. In experiment 1, two dietary treatments were fed from 4 to 11 d of age. Dietary treatments consisted of a control diet (no added glycerin) and a diet containing 6% glycerin (94% control diet + 6% glycerin). Four dietary treatments were provided in experiment 2 (from 17 to 24 d of age) and 3 (from 38 to 45 d of age). Diets in experiment 2 and 3 were 1) control diet (no added glycerin); 2) 3% added glycerin (97% control diet + 3% glycerin); 3) 6% added glycerin (94% control diet + 6% glycerin); and 4) 9% added glycerin (91% control diet + 9% glycerin). Diets in experiment 1 and 2 were identical, but the diet used in experiment 3 had reduced nutrient levels based on bird age. In experiments 2 and 3, broilers were fed 91, 94, 97, and 100% of ad libitum intake so that differences in AMEn consumption were only due to glycerin. A single source of glycerin was used in all experiments. Feed intake, BW, energy intake, energy excretion, nitrogen intake, nitrogen excretion, AMEn, and AMEn intake were determined in all experiments. In experiment 1, AMEn determination utilized the difference approach by subtracting AMEn of the control diet from AMEn of the test diet. In experiments 2 and 3, AMEn intake was regressed against feed intake with the slope estimating AMEn of glycerin. Regression equations were Y = 3,331x -72.59 (P < or = 0.0001) and Y = 3,348.62x -140.18 (P < or = 0.0001) for experiments 2 and 3, respectively. The AMEn of glycerin was determined as 3,621, 3,331, and 3,349 kcal/kg in experiments 1, 2, and 3, respectively. The average AMEn of glycerin across the 3 experiments was 3,434 kcal/kg, which is similar to its gross energy content. These results indicate that AMEn of glycerin is utilized efficiently by broiler chickens.

The energy value of crude glycerin from different biodiesel production facilities was determined in nursery pigs (initial BW of 10.4 kg) to predict apparent DE and ME based on the composition of crude glycerin. Dietary treatments consisted of a basal diet, or diets containing crude glycerin from various biodiesel production facilities supplemented in the diet at approximately 9.1%. Because of bulk density differences, 2 glycerin products were supplemented at either 7.7 or 6.9%. In addition, soybean oil and lard were included at 6.7% as 2 dietary treatments to serve as positive controls. Each diet was fed twice daily to pigs in individual metabolism crates. After a 6-d adjustment period, a 4-d balance experiment was conducted. During the collection period, feces and urine were collected daily and stored at 0 degrees C until analysis. The GE of each test ingredient and diet and of urine and fecal samples from each pig were determined by isoperibol bomb calorimetry. The DE and ME values of crude glycerol were estimated by difference, whereby the DE and ME content of the basal diet was subtracted from the complete diet containing the test ingredient. Gross energy, DE, and ME of US Pharmacopeia grade glycerin were determined to be 4,325, 4,457, and 3,682 kcal/kg, respectively. In contrast, GE of the crude glycerin samples ranged from 3,173 to 6,021 kcal/kg, DE ranged from 3,022 to 5,228 kcal/kg, and ME ranged from 2,535 to 5,206 kcal/kg, reflecting the content of glycerol, methanol, and FFA in the crude glycerin. The GE, DE, and ME of soybean oil and lard were determined to be 9,443, 8,567, and 8,469 kcal/kg, and 9,456, 8,524, and 8,639 kcal/kg, respectively. The stepwise regression prediction of the ME in crude glycerin exhibited R(2) of only 0.41 [ME, kcal/kg (as-is basis) = (37.09 x % of glycerin) + (97.15 x % of fatty acids)], whereas prediction of GE achieved an R(2) of 0.99 [GE, kcal/kg (as-is basis) = -236 + (46.08 x % of glycerin) + (61.78 x % of methanol) + (103.62 x % of fatty acids)]. On average, the ME of crude glycerin was 85.4% of its GE (SE 5.3) and did not differ by glycerin source. The data provided in these experiments indicate that crude glycerin is a valuable energy source, with its GE concentration dependent on the concentration of glycerin, methanol, and fatty acids, and with ME as a percentage of GE averaging 85.4%.

No abstract

Two experiments were conducted to evaluate the effect of in ovo amino acid (AA) injections in broiler breeder eggs on AA utilization of embryos. All AA used in these experiments were pure crystalline AA in free-base form. Treatments in Experiment 1 comprised 1) control eggs (no injection), 2) 0.5 mL sterile-distilled water injected eggs, and 3) eggs injected with an AA solution suspended in 0.5 mL sterile-distilled water. Injections were administered into the yolk at Day 7 of incubation. At hatch, chicks were killed and bled, and plasma AA concentration was determined. Plasma AA concentration of hatched chicks decreased (P < 0.05) when water was injected. In addition, all AA from eggs injected with AA, except Glu and Lys, were decreased (P < 0.05) at hatch as compared to control eggs. However, AA pattern was not affected by in ovo water injection, but the AA ratio to Lys was reduced by in ovo AA injection. Experiment 2 was conducted to evaluate whole internal egg AA concentrations over incubation time in the presence or absence of in ovo AA administration. Treatments in Experiment 2 comprised 1) control eggs (no injection), and 2) eggs injected with a AA solution at Day 7 of incubation. The AA contents of embryo, yolk, albumen, and allantoic and amnion fluids were analyzed over time during incubation (Days 0, 7, 14, and 19 of incubation). On Day 14 of incubation, there were no differences in AA contents of all tissues between the control group and the group injected with AA on Day 7 of incubation. On Day 19 of incubation, AA contents of embryo, yolk, albumen, and allantoic and amnion fluids were increased (P < 0.05) as mediated by in ovo administration of AA at Day 7 of incubation. These results suggest that in ovo administration of AA may increase AA concentrations in chicken embryos and other egg contents.