Growth Performance of Broilers in Response to Increasing Concentration of Multiple Mycotoxins in Contaminated Corn

Mycotoxins in grains are a result of mold or fungal growth from environmental stressors and cause detrimental impacts to poultry production. Thus, the objective of this experiment was to determine the effects of increasing concentration of a combina­tion of mycotoxins on growth performance of broiler chicks. A total of 250 one-day-old male broilers (Cobb 500; initial BW 0.092 lb) were used in a 15-d study. Broilers were housed in 3 Petersime batteries with ad libitum access to feed and water. Treatments were randomly assigned to 1 of 50 cages within location block, resulting in 10 cages per treatment with 5 broilers per cage balanced by BW. For this experiment, the sourced contaminated corn contained 8.2 ppm fumonisin (FUM), 8.0 ppm deoxynivalenol (DON), and 551 ppb zearalenone (ZEA). Dietary treatments consisted of 0%, 25%, 50%, 75%, and 100% of the mycotoxin contaminated corn replacing non-contaminated corn. The resulting complete diet mycotoxin concentrations were 1.5 ppm, 1.4 ppm, 2.3 ppm, 2.9 ppm, and 3.9 ppm for FUM; \u3c 0.6 ppm, 1.0 ppm, 1.4 ppm, 2.3 ppm, and 3.0 ppm for DON; and \u3c 51.7 ppb, 94.5 ppb, 180.5 ppm, 294.6 ppb, and 364.1 ppb for ZEA, respectively. Data were analyzed as a completely randomized design with cage as the experimental unit using the GLIMMIX procedure of SAS 9.4 (Cary, NC). Results were considered significant at P ≤ 0.05. Total body weight gain (BWG) decreased (linear, P = 0.007) and feed intake (FI) tended to decrease (linear, P = 0.093) in broilers fed diets with increasing concentration of mycotoxin contaminated corn in the diet. The increase in mycotoxin concentration in diets fed to broilers also resulted in poorer (linear, P = 0.010) feed conversion ratio (FCR). In conclusion, increasing concentra­tions of FUM, DON, and ZEA in broiler feed negatively impacted BWG, FI, and FCR even when the mycotoxin levels were below acceptable limits for individual mycotoxins

Effect of Metabolizable Energy and Crumble Quality of the Diet on Growth Performance of Broilers

In order to optimize the growth performance of broilers, diets are formulated to a recommended ME concentration. In addition, broilers (chicks) are often fed diets in the form of crumbles in early production to improve growth performance. Thus, the objective of this study was to determine the effect of ME concentration in diets and if removal of crumble fines influenced the growth performance response of broilers. At hatch, a total of 300 one-day-old male broilers (Cobb 500, initial BW 0.093 lb) were used in an 18-day study. Broilers were housed in 3 Petersime batteries with ad libitum access to feed and water. Treatments were randomly assigned to 60 cages balanced by location, resulting in 10 cages per treatment with 5 broilers per cage. Treatments were arranged in a 2 × 3 factorial of ME content (1,376 and 1,346 ME, kcal/lb) and crumbled diets with or without fines (removed particles \u3c 1,532 µm or \u3c 864 µm). Crumble treatments were fed with no sifting (NS) or sifted using either a screen with 0.06-in. openings (removed particles \u3c 1,532 µm) or a screen with 0.03-in. openings (removed particles \u3c 864 µm). Data were analyzed as a completely randomized design using the GLIMMIX procedure of SAS (v. 9.4, SAS Institute, Inc., Cary, NC). There was no evidence of an interaction between crumble fines removal and ME or main effect of ME. Body weight gain (BWG) and total feed intake (TFI) increased (P \u3c 0.05) when broilers were fed crumbles sifted with a 0.06-in. screen compared to NS and crumbles sifted with a 0.03-in. screen. Broiler feed conversion ratio (FCR) improved (P \u3c 0.001) when broilers were fed crumbles sifted with a 0.06-in. screen compared to those fed NS and sifted with a 0.03-in. screen. In conclusion, broilers fed crumbles with particles \u3c 1,532 µm removed had an improved FCR and an increased BWG and TFI regardless of the ME content of the diet. Increasing ME from 1,346 to 1,376 kcal/lb did not influence growth performance of broilers from d 0 to 18 d of age

Effects of Maternal Choline Supplementation On Offspring Self-Regulation: Results of Two Randomized Controlled Trials

245 pagesBackground and Objective: Choline, an essential nutrient, has many important roles during pregnancy. However, most women do not consume the Adequate Intake (AI), and choline is not currently part of standard prenatal regimens. A large body of rodent research has demonstrated that maternal choline intake beyond amounts in standard rodent chow is important for offspring cognition throughout the lifespan, especially attention and memory. There is preliminary evidence to suggest the translation of these effects to humans, although important gaps in our knowledge remain, two of which are addressed by this dissertation. First, no prior studies have experimentally manipulated maternal choline intake and followed the children to school-age; the first chapter of this dissertation presents the results of a test of executive functioning administered to the 7-year-old children of women who participated in a controlled choline feeding study. Second, although a small body of rodent research suggests that maternal choline intake may be important for offspring socioemotional function, no human studies have evaluated the effects of maternal choline intake on infant socioemotional outcomes; chapters 2 and 3 of this dissertation, respectively, present results from a study of maternal choline supplementation on indices of infant temperament and affect regulation during the first year of life. Methods: Childhood Study: Third-trimester pregnant women were recruited to take part in a randomized controlled feeding trial. Women were randomized to consume either 480 mg/day (approximately the AI) or 930 mg/day choline until delivery. An ancillary follow-up study was conducted when their children were 7 years old to assess attention, memory, and executive functioning. This thesis presents the results of the Tower of London, an executive function task of planning and problem-solving. Infancy Study: Second-trimester pregnant women were recruited to take part in a randomized controlled supplementation trial. Women were randomized to consume either 25 mg/day or 550 mg/day choline, plus usual diet, until delivery. An ancillary follow-up study was conducted when their infants were 5–13 months old to assess attention, memory, and socioemotional functioning. This thesis presents the results of the Infant and Early Childhood Behavior Questionnaires and the Face-to-Face Still Face Paradigm. Results: Childhood Study: In the childhood study (N = 20), children whose mothers consumed 930 mg/day choline performed better on a task of planning and problem-solving skills as compared to children whose mothers consumed 480 mg/day choline, indicative of superior executive functioning. Infancy Study: In the infancy study, there was no effect of maternal choline supplementation on parent-report measures of infant temperament (N = 25) across the first year of life or on a laboratory measure of affect regulation at 7 months of age (N = 16). Conclusions: Childhood Study: Maternal choline supplementation at approximately 2x the AI has significant beneficial effects on child executive functioning at 7 years of age compared to the AI. Infancy Study: Maternal choline supplementation in addition to usual diet does not have an effect on infant temperament or affect regulation. However, interesting patterns emerged indicative of a more adaptive affective response in the infants born to women in the higher choline supplementation group. These preliminary data indicate that the current AI for pregnant women may not be sufficient for offspring self-regulation and support the conclusion that choline should be added to a standard prenatal vitamin regimen

Prenatal choline supplementation improves biomarkers of maternal docosahexaenoic acid (DHA) status among pregnant participants consuming supplemental DHA: a randomized controlled trial

BackgroundDietary methyl donors (e.g., choline) support the activity of the phosphatidylethanolamine N-methyltransferase (PEMT) pathway, which generates phosphatidylcholine (PC) molecules enriched in DHA that are exported from the liver and made available to extrahepatic tissues.ObjectivesThis study investigated the effect of prenatal choline supplementation on biomarkers of DHA status among pregnant participants consuming supplemental DHA.MethodsPregnant participants (n = 30) were randomly assigned to receive supplemental choline intakes of 550 mg/d [500 mg/d d0-choline + 50 mg/d deuterium-labeled choline (d9-choline); intervention] or 25 mg/d (25 mg/d d9-choline; control) from gestational week (GW) 12-16 until delivery. All participants received a daily 200-mg DHA supplement and consumed self-selected diets. Fasting blood samples were obtained at baseline, GW 20-24, and GW 28-32; maternal/cord blood was obtained at delivery. Mixed-effects linear models were used to assess the impact of prenatal choline supplementation on maternal and newborn DHA status.ResultsCholine supplementation (550 vs. 25 mg/d) did not achieve a statistically significant intervention × time interaction for RBC PC-DHA (P = 0.11); a significant interaction was observed for plasma PC-DHA and RBC total DHA, with choline supplementation yielding higher levels (+32-38% and +8-11%, respectively) at GW 28-32 (P < 0.05) and delivery (P < 0.005). A main effect of choline supplementation on plasma total DHA was also observed (P = 0.018); its interaction with time was not significant (P = 0.068). Compared with controls, the intervention group exhibited higher (P = 0.007; main effect) plasma enrichment of d3-PC (d3-PC/total PC). Moreover, the ratio of d3-PC to d9-PC was higher (+50-67%; P < 0.001) in the choline intervention arm (vs. control) at GW 20-24, GW 28-32, and delivery.ConclusionsPrenatal choline supplementation improves hepatic DHA export and biomarkers of DHA status by bolstering methyl group supply for PEMT activity among pregnant participants consuming supplemental DHA. This trial is registered at www.clinicaltrials.gov as NCT03194659