Related Experiment Video
Updated: Jun 9, 2026
In Ovo Feeding of Commercial Broiler Eggs: An Accurate and Reproducible Method to Affect Muscle Development and Growth
Published on: September 20, 2021
Effects of early neonatal development and delayed feeding immediately post-hatch on the hepatic lipogenic program in
Mark P Richards1, Monika Proszkowiec-Weglarz, Robert W Rosebrough
1United States Department of Agriculture, Agricultural Research Service, Animal and Natural Resources Institute, Beltsville, MD 20705-2350, USA. Mark.Richards@ars.usda.gov
Insights
Early feeding in broiler chickens is crucial for establishing lipogenic gene expression. Delayed feeding post-hatch significantly depresses body weight gain and inhibits key gene activation necessary for growth and metabolism.
Area of Science:
- Animal Science
- Developmental Biology
- Molecular Biology
Background:
- The transition from embryonic to neonatal life is critical for broiler development, influencing metabolic and growth programming.
- Hepatic lipogenesis, the process of fatty acid synthesis in the liver, is a key metabolic pathway regulated by specific genes.
Purpose of the Study:
- To investigate the effects of early post-hatch (PH) development on the activation of hepatic lipogenesis genetic programs.
- To determine the impact of delayed feeding initiation on lipogenic gene expression and broiler growth.
Main Methods:
- Oligonucleotide-based chicken genome microarrays were used to compare liver RNA at hatch and 7 days PH.
- Gene-specific RT-PCR assays confirmed microarray findings.
- Delayed feeding (48 hours PH) was implemented in a follow-up study to assess its effects on lipogenic gene expression and physiological parameters.
Main Results:
- Key lipogenic genes (e.g., ACL, ME, FAS, ACCα, SCD-1, SREBP-2, Spot 14α) were significantly up-regulated during the first week PH.
- Delayed feeding (DF) significantly depressed body weight gain and inhibited the up-regulation of lipogenic genes until feeding commenced.
- While metabolic hormones (insulin, glucagon, T3) changed during PH development, they were largely unaffected by DF; plasma glucose was transiently lower in the DF group.
Conclusions:
- Early post-hatch development involves significant transcriptional programming of hepatic lipogenesis.
- Initiation of feeding post-hatch is critical for the timely activation of lipogenic genes and optimal broiler growth.
- Delayed feeding disrupts normal metabolic programming, highlighting the importance of early nutrition in broiler development.
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 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 days PH was performed using oligonucleotide-based (Affymetrix GeneChip®) chicken genome microarrays. During the first week 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 (ACCα), stearoyl-CoA desaturase-1 (SCD-1), sterol regulatory element binding protein-2 (SREBP-2) and thyroid hormone responsive spot 14α (Spot 14α) 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 days PH. Body weight gain was significantly depressed by DF. Plasma levels of the major metabolic hormones that regulate lipogenic gene expression (insulin, glucagon and T(3)) changed significantly during PH development, but were largely unaffected by DF. Plasma glucose was significantly lower in the DF group at 24h 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 (PPARγ), 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.
