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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Animal Biosciences & Biotechnology Laboratory » Research » Publications at this Location » Publication #379576

Research Project: Novel Integrated Nutrition and Health Strategies to Improve Production Efficiencies in Poultry

Location: Animal Biosciences & Biotechnology Laboratory

Title: The effect of delayed feeding post-hatch on ceca development in broiler chickens

item QU, YANG - University Of Maryland
item Kahl, Stanislaw
item Miska, Kate
item Shannon, Amy
item Russell, Beverly
item ELSASSER, THEODORE - Retired ARS Employee
item Proszkowiec-Weglarz, Monika

Submitted to: British Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/18/2021
Publication Date: 4/9/2021
Citation: Qu, Y., Kahl, S., Miska, K.B., Shannon, A.E., Russell, B.A., Elsasser, T.H., Proszkowiec-Wegla, M.K. 2021. The effect of delayed feeding post-hatch on ceca development in broiler chickens. British Poultry Science.

Interpretive Summary: In the current broiler production systems, chicks are deprived of food and water for up to 72 hours due to uneven hatching, hatchery procedures such as sexing, sorting, selection and vaccination, and transportation time to destination farms. Lack of access to feed during the first 48-72 hours results in lower body and organ weight, higher feed conversion ratio (amount of feed required for 1kg of body weight gain) and mortality, delayed growth rate and gastrointestinal tract development. Little is known about the effects of early neonatal development and delayed feeding immediately post-hatch on ceca development in chickens. Ceca is the biggest reservoir of microflora in the gastrointestinal tract and mainly plays a role in fermentation of undigested carbohydrates to short chain fatty acids. Therefore, the aim of the present study was to characterize mRNA and protein expression pattern of gut barrier-, immune function-, nutrient transport- and mitochondria-related genes in ceca of broiler chickens during early development and delayed access to feed post-hatch. To mimic commercial settings, newly hatched chicks were subjected to 48 hours delay in feeding or fed immediately after hatch. We have determined that delayed access to feed immediately post-hatch has limited effect on developmental changes in ceca function. Our results suggest that ceca seem to be resistant to delayed access to feed early post-hatch with only few genes affected.

Technical Abstract: Broiler chicks are frequently deprived of food up to 72 h due to uneven hatching, hatchery procedures, and transportation to farms. Little is known about the effect of delayed feeding immediately post-hatch (PH) on the early neonatal development of the ceca. Therefore, the objective of this study was to investigate the developmental changes and effects of a 48-h delay in feed access immediately PH on the ceca. Ross 708 eggs (250) were incubated under standard conditions. After hatch, birds were randomly divided into two treatment groups (n=6 battery pen/treatment). One group (F) received feed and water immediately after hatch, while the second group (NF) had access to water but had delayed access to feed for 48 h. Medial regions of the ceca were collected for mRNA expression as well as for histological analysis at several time points. Expression of MCT-1 (nutrition transporter), Cox7A2 (mitochondria function) IgA, pIgR, and ChIL-8 (immune functions) genes were affected by interaction of age and delayed access to feed. Expression of LEAP2 and MUC2 was increased in NF group. There was no effect of feed delay on expression of genes related to mitochondrial functions in ceca, although developmental changes were observed (ATP5F1B, Cox4|1). Histological changes during ceca development were affected by delayed access to feed. Our data suggest a limited effect of delayed feed access PH on the developmental changes in cecal functions. The data also indicate that ceca seem to be resistant to delayed access to feed early PH with only a few genes affected.