|Proszkowiec-Weglarz, M -|
|Angel, R -|
Submitted to: Poultry Science Meeting
Publication Type: Abstract Only
Publication Acceptance Date: April 14, 2009
Publication Date: May 29, 2009
Citation: Richards, M.P., Proszkowiec-Weglarz, M., Rosebrough, R.W., Mcmurtry, J.P., Angel, R. 2009. Effects of early neonatal development and delayed feeding immediately post-hatch on the hepatic lipogenic program [abstract]. Poultry Science. Abstract Number 394P Technical Abstract: 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 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 the Affymetrix chicken genome array. 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 a (ACCa), stearoyl-CoA desaturase-1 (SCD-1), sterol regulatory element binding protein-2 (SREBP-2) and thyroid hormone responsive spot 14 (S14) 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 and SREBP-2, 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.