Abstract
Hepatic gluconeogenesis is the main source of glucose during chicken embryonic development, and it plays a major role in glucose homeostasis for developing embryos. Phosphoenolpyruvate carboxylase (PEPCK) catalyzes the rate-limiting step of gluconeogenesis, yet how hepatic PEPCK expression is differentially regulated between chicken breeds remains elusive. In this study, fertile eggs from a slow-growing Chinese Yellow Feathered Chicken and a fast-growing White Recessive Rock Chicken were incubated under the same standard conditions, and serum and liver samples were collected on embryonic d 18 (18E). The fast-growing breed had a significantly higher fetal weight (P < 0.01) and serum glucose concentration (P < 0.05) compared with the slow-growing breed. The fast-growing breed also had significantly higher hepatic mRNA expression levels of the cystolic form of PEPCK (PEPCK-c; P < 0.05) and significantly higher hepatic mRNA and protein expression levels of cAMP response element binding protein 1 (CREB-1; P < 0.05). Moreover, the binding of phosphorylated CREB-1 to the PEPCK-c promoter tended to be higher in the fast-growing breed (P = 0.08). Breed-specific epigenetic modifications of the PEPCK-c promoter were also observed; the fast-growing breed demonstrated lower CpG methylation (P < 0.05) and histone H3 (P < 0.05) levels but more histone H3 acetylation (H3ac) and histone H3 lysine 27 trimethylation (H3K27me3; P < 0.05) compared with the slow-growing breed. Our results suggest that hepatic PEPCK-c expression is transcriptionally regulated in a breed-specific manner and that fast- and slow-growing broiler chicken fetuses exhibit different epigenetic modifications on their PEPCK-c promoter regions.