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 β-hydroxy-β-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.

Accessory to Obesity?: Melanocortin receptors are a family of cell membrane receptors that control diverse physiological functions. Mutations in the gene encoding melanocortin 4 receptor (MC4R) are a cause of familial early-onset obesity. Asai et al. (p. 275 ) studied the function of an accessory protein for MC4R signaling, MRAP2, and found that mice genetically deficient in MRAP2 develop severe obesity. Sequencing of MRAP2 in unrelated, severely obese humans revealed one individual with a clearly disruptive genetic variant, suggesting that MRAP2 mutations might also be a rare cause of human obesity. In a zebrafish model, Sebag et al. (p. 278 ) studied two paralogs of the MRAP2 accessory protein, one of which enhanced MC4R responsiveness to α–melanocyte-stimulating hormone, which regulates feeding and growth.

The effects of 2 levels of mannanoligosaccharide (MOS) in feed were compared with antibiotic growth promoters on growth performance, intestinal morph

Four hundred and fifty 1-d-old male Lingnan Yellow broiler chickens were used to investigate the effects of Clostridium butyricum on growth performan

The amount of nutrients (i.e., N, P, Zn, and Cu) and associated odors emitted from production animals into the environment can be modulated by several different nutritional strategies, but their practical application is dependent on costs and biological limitations. In general, nutrient excretion may be reduced by avoiding the overfeeding of specific nutrients or by using nutritional manipulations to enhance nutrient utilization in the animal. Loss to the environment can be avoided by manufacturing and handling the feed in a pelletized form that will minimize waste and improve feed/gain. Other strategies for minimizing nutrient losses include: 1) the development of feeding programs that are specific for sex and strain of the animal; 2) increasing the number of feed phases to better meet the animal's age-related requirements; 3) formulating diets to include the minimal amounts of nutrients required to satisfy production goals; 4) meeting the animal's amino acid requirements; 5) using synthetic amino acid supplements to feed to reduce N emission; 6) using feed ingredients with high digestibility and nutrient bioavailability; and 7) formulating diets based on nutrient availability instead of total nutrient content. Nutrient digestibility of feedstuffs is dependent on processing conditions, genetic characteristics of the grains and oilseeds, and the presence of nutritional antagonists in specific feedstuffs used in the diet. Feed ingredients that lead to odor production can be avoided (e.g., fishmeal and some easily fermentable feed ingredients). Feed additives, such as antibiotics, nonstarch polysaccharides, direct-fed microbials, organic acids, microbial enzymes (i.e., phytase, carbohydrases, and proteases) can be used to increase the digestibility and absorption of nutrients or to modulate the microflora. Finally, a cost factor for the control or disposal of nutrients or odor should be considered in the feed formulation to optimize the various nutritional strategies discussed above. Regardless of biological and economic limitations, significant reductions in nutrient and odor emission from nonruminants can be achieved by appropriate nutritional strategies, but response may differ for swine and poultry. Copyright © 2002. American Society of Animal Science . ©2002 American Society of Animal Science

The protective mucus layer covers the entire surface of the gastrointestinal tract. The mucus layer also acts as a medium for molecule transport between the luminal contents and the enterocytes; therefore it has a major role in nutrient absorption. The main mucus layer component, mucin glycoproteins, is produced by mucous-secreting goblet cells. In chicken small intestine, functional development of goblet cells and enterocytes occurs in the late embryonic and immediate posthatch period. Presence of the nutrient is crucial for mucosal development. Feed deprivation immediately after hatch caused delayed mucosa development and perturbed mucin dynamics. Recent studies showed the intraamnionic nutrient supply (in-ovo feeding; IOF) accelerated mucosa functional development. In this study, the effect of IOF on the mucin mRNA expression and mucin content in the goblet cells was studied. The feeding solution containing carbohydrates was administered to the amnionic fluid of the Cobb embryos at d 17.5 of incubation. Samples from the jejunum were taken at d 17 of incubation (before IOF), and then 10 embryos from each group were sampled at 19 d of incubation, at hatch, and at d 3 posthatch. Following IOF, villus surface area increased at day of hatch and 3 d posthatch by 27 and 21%, respectively. In addition, the proportion of goblet cells containing acidic mucin increased 36 h after injection by 50% compared with the controls. The mucin mRNA expression increased gradually from d 17 of incubation to 3 d posthatch. Enhanced expression of the mucin mRNA was found at the day of hatch in chicks that received carbohydrate solution into the amnionic fluid in comparison with the control group. The results showed that providing the carbohydrates as an energy source to the late-term embryo had a trophic effect on the small intestine and enhanced goblet cell development.