In ovo feeding improves energy status of late-term chicken embryos.

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.