Delayed access to feed affects broiler small intestinal morphology and goblet cell ontogeny.

Broilers are often deprived of feed and water for up to 48 h after hatch. This delayed access to feed (DAF) can inhibit small intestine development. The objective of this study was to determine the effects of DAF on small intestinal morphology, mRNA abundance of the goblet cell marker Muc2 and absorptive cell marker PepT1, and the distribution of goblet cells in young broilers. Cobb 500 chicks, hatching within a 12-h window, were randomly allocated into 3 groups: control with no feed delay (ND), 24-h feed delay (DAF24), and 36-h feed delay (DAF36). Morphology, gene expression, and in situ hybridization analyses were conducted on the duodenum, jejunum, and ileum at 0, 24, 36, 72, 120, and 168 h after hatch. Statistical analysis was performed using a t test for ND and DAF24 at 24 h. A 2-way ANOVA and Tukey's HSD test (P < 0.05) were used for ND, DAF24, and DAF36 from 36 h. At 24 to 36 h, DAF decreased the ratio of villus height/crypt depth (VH/CD) in the duodenum but increased VH/CD in the ileum due to changes in CD, whereas at 72 h, DAF decreased VH/CD due to a decrease in VH. The mRNA abundance of PepT1 was upregulated, while Muc2 mRNA was downregulated in DAF chicks. Cells expressing Muc2 mRNA were present along the villi and in the crypts. The ratio of the number of goblet cells found in the upper half to the lower half of the villus was greater in DAF chicks than in ND chicks, suggesting that DAF affected the appearance of new goblet cells. The number of Muc2 mRNA-expressing cells in the crypt, however, was generally not affected by DAF. In conclusion, DAF transiently affected small intestinal morphology, upregulated PepT1 mRNA, downregulated Muc2 mRNA, and changed the distribution of goblet cells in the villi. By 168 h, however, these parameters were not different between ND, DAF24, and DAF36 chicks.