Maintenance of glucose homeostasis during late-term embryonic development is dependent upon the amount of glucose held in reserve primarily in the form of glycogen in the liver and upon the degree of glucose generated by gluconeogenesis from protein first mobilized from amnion albumen and then from muscle. Insufficient glycogen and albumen will force the embryo to mobilize more muscle protein toward gluconeogenesis, thus restricting growth of the late-term embryo and hatchling. We hypothesize that administration of available carbohydrates to the amnion will improve glycogen reserves and spare muscle protein mobilization for gluconeogenesis during late-term embryonic and posthatch neonatal development. Our hypothesis was tested by comparing BW gain, liver glycogen reserves, and muscle weight of in ovo fed and control embryos during last days of embryonic incubation until 25 d after hatching. We examined, using 600 birds from 2 different strains of commercial boilers, body and muscle weights and glycogen reserves following feeding embryos at d 17.5 of incubation with a solution containing maltose, sucrose, dextrin, and beta-hydroxy-beta-methylbutyrate (HMB). Providing carbohydrates and HMB to late-term embryos increased hatching weights by 5 to 6% over controls, improved liver glycogen by 2- to 5-fold, and elevated relative breast muscle size by 6 to 8%. These weight advantages were sustained through the end of the experiments at 25 d of age. It is reasonable to assume that the elevated glycogen levels in the in ovo treatment reduce the need to produce glucose via gluconeogenesis and, therefore, contribute to less use of muscle protein and hence a greater percentage of pectoral muscle weight in the in ovo birds.

Zinc (Zn) deficiency is a prevalent micronutrient insufficiency. Although the gut is a vital organ for Zn utilization, and Zn deficiency is associated with impaired intestinal permeability and a global decrease in gastrointestinal health, alterations in the gut microbial ecology of the host under conditions of Zn deficiency have yet to be studied. Using the broiler chicken (Gallus gallus) model, the aim of this study was to characterize distinct cecal microbiota shifts induced by chronic dietary Zn depletion. We demonstrate that Zn deficiency induces significant taxonomic alterations and decreases overall species richness and diversity, establishing a microbial profile resembling that of various other pathological states. Through metagenomic analysis, we show that predicted Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways responsible for macro- and micronutrient uptake are significantly depleted under Zn deficiency; along with concomitant decreases in beneficial short chain fatty acids, such depletions may further preclude optimal host Zn availability. We also identify several candidate microbes that may play a significant role in modulating the bioavailability and utilization of dietary Zn during prolonged deficiency. Our results are the first to characterize a unique and dysbiotic cecal microbiota during Zn deficiency, and provide evidence for such microbial perturbations as potential effectors of the Zn deficient phenotype.

Early development of the digestive tract is crucial for achieving maximal growth and development of chickens. Because the late-term embryo naturally consumes the amniotic fluids, insertion of a nutrient solution into the embryonic amniotic fluid [in ovo (IO) feeding] may enhance development. This study examined the effect of IO feeding on d 17.5 of incubation of carbohydrates (CHO) and beta-hydroxy-beta-methylbutyrate (HMB) on small intestinal development of chickens during the pre and posthatch periods. Results shows that 48 h post-IO feeding procedure all IO feeding treatments exhibited increased villus width and surface area compared with the control group. At d 3 posthatch the surface area of an average villi was increased by 45% for the HMB IO group and by 33% for the CHO and CHO+HMB IO groups compared with controls (noninjected fertile eggs). The activity of jejunal sucrase-isomaltase (SI) was higher (P < 0.05) 48 h after IO feeding in all the IO fed embryos, whereas at day of hatch and at d 3 the CHO+HMB IO group had the highest maltase activity (P < 0.05), which was approximately 50% greater than control embryos. These observations indicated that small intestines of IO fed hatchlings were functionally at a similar stage of development as a conventionally fed 2-d-old chick. Body weight of all IO fed hatchlings was greater than controls, and these differences (P < 0.05) were sustained until the end of the experiment (10 d). At d 10 chicks that were IO fed with CHO had BW that were 2.2% higher, whereas HMB and CHO+HMB IO fed chicks showed 5 to 6.2% BW increase, respectively, compared with controls. The current study shows that the administration of exogenous nutrients into the amnion enhanced intestinal development by increasing the size of the villi and by increasing the intestinal capacity to digest disaccharides. This advantage probably leads to higher BW in IO fed chicks.

The use of engineered nanoparticles in food and pharmaceuticals is expected to increase, but the impact of chronic oral exposure to nanoparticles on human health remains unknown. Here, we show that chronic and acute oral exposure to polystyrene nanoparticles can influence iron uptake and iron transport in an in vitro model of the intestinal epithelium and an in vivo chicken intestinal loop model. Intestinal cells that are exposed to high doses of nanoparticles showed increased iron transport due to nanoparticle disruption of the cell membrane. Chickens acutely exposed to carboxylated particles (50 nm in diameter) had a lower iron absorption than unexposed or chronically exposed birds. Chronic exposure caused remodelling of the intestinal villi, which increased the surface area available for iron absorption. The agreement between the in vitro and in vivo results suggests that our in vitro intestinal epithelium model is potentially useful for toxicology studies.