INVESTIGATION OF GENETIC MECHANISMS FOR IMPROVING THE REGULATION OF FEED INTAKE AND NUTRIENT UTILIZATION IN POULTRY
Title: Effects of early neonatal development and delayed feeding immediately post-hatch on the hepatic lipogenic program in broiler chicks
| Richards, Mark |
| Proszkowiec-Weglarz, Monika - |
| Rosebrough, Robert |
| Angel, Roselina - |
Submitted to: Comparative Biochemistry and Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 26, 2010
Publication Date: December 1, 2010
Citation: Richards, M.P., Proszkowiec-Weglarz, M., Rosebrough, R.W., McMurtry, J.P., Angel, R. 2010. Effects of early neonatal development and delayed feeding immediately post-hatch on the hepatic lipogenic program in broiler chicks. Comparative Biochemistry and Physiology. 157(Part B):374-388.
Interpretive Summary: The first week post-hatch is a crucial period of growth and development for broiler chickens. How well the broiler chick transitions from utilizing nutrients provided from the egg contents (especially high fat yolk) to those provided from a high carbohydrate low fat feed consumed shortly after hatching determines not only its survival, but also its subsequent performance during the remainder of the production cycle. Since fat is an important energy source, it is vital that the newly hatched chick quickly develop the ability to regulate the production, utilization and storage of the requisite amount of fat required for optimal growth and development. Therefore, the goal of this work was to relate changes in the functioning of individual genes and gene networks with the metabolic adaptations that occur in response to initiation of feed consumption right after hatch in broiler chickens. To do this we utilized global gene expression analysis encompassing the entire chicken genome to evaluate unique gene functions in liver, a key organ involved in regulating fat metabolism in the chicken. Our analysis revealed that a variety of genes involved in fatty acid, cholesterol and carbohydrate metabolism were coordinately activated with the onset of feed consumption during the first week after hatching. Some of these genes had been previously identified and studied while others were found to be new candidates for further study. The results from this work will help define genetic mechanisms that regulate the post-hatch metabolic transition in broiler chicks and suggest possible nutritional and management approaches to optimize broiler performance during this critical time of production. This information is useful to researchers studying the control of fat metabolism in avian species, as well as, to poultry producers in formulating new genetic selection and feeding strategies for use in commercial poultry flocks.
The embryo to neonate transition is a critical period of development that has significant impact on broiler production. During this time important genetic programs governing metabolism and growth are established. The goal of this work was to study the effects of early post-hatch (PH) development and the time of initiation of feeding on activation of the genetic program regulating hepatic lipogenesis. A comparison of liver total RNA samples at hatch and 7 d PH was performed using oligonucleotide-based (Affymetrix GeneChip) chicken genome microarrays. During the first wk PH there was significant up-regulation of key lipogenic genes including: ATP citrate lyase (ACL), malic enzyme (ME), fatty acid synthase (FAS), acetyl-CoA carboxylase alpha (ACCa), stearoyl-CoA desaturase-1 (SCD-1), sterol regulatory element binding protein-2 (SREBP-2) and thyroid hormone responsive spot 14a (Spot 14a) among others. These findings were confirmed using gene-specific RT-PCR assays. In a follow-up study, we investigated the effects of withholding feed for the first 48 h PH (delayed feeding, DF) on lipogenic gene expression through 8 d PH. Body weight gain was significantly depressed by DF. Plasma levels of the major metabolic hormones that regulate lipogenic gene expression (insulin, glucagon and T3) changed significantly during PH development, but were largely unaffected by DF. Plasma glucose was significantly lower in the DF group at 24 h PH but recovered thereafter. In general, DF inhibited the up-regulation of lipogenic genes until feeding was initiated. Delayed up-regulation was also observed for the lipogenic transcription factor genes, SREBP-1, SREBP-2 and peroxisome proliferator-activated receptor gamma (PPARg), but not for carbohydrate response element binding protein (ChREB) or liver X receptor (LXR). Our results offer additional insight into the transcriptional programming of hepatic lipogenesis in response to the transition from high fat (yolk) to high carbohydrate (feed) nutrition that occurs during early PH development.