Delayed Feeding Alters Transcriptional and Post-Transcriptional Regulation of Hepatic Metabolic Pathways in Peri-Hatch Broiler Chicks.

Julie A. Hicks,Nishanth E. Sunny,Tom E. Porter,Hsiao-Ching Liu

doi:10.3390/genes10040272

Julie A. Hicks, Nishanth E. Sunny + Show 2 more

Open Access

https://doi.org/10.3390/genes10040272

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Abstract

Hepatic fatty acid oxidation of yolk lipoproteins provides the main energy source for chick embryos. Post-hatching these yolk lipids are rapidly exhausted and metabolism switches to a carbohydrate-based energy source. We recently demonstrated that many microRNAs (miRNAs) are key regulators of hepatic metabolic pathways during this metabolic switching. MiRNAs are small non-coding RNAs that post-transcriptionally regulate gene expression in most eukaryotes. To further elucidate the roles of miRNAs in the metabolic switch, we used delayed feeding for 48 h to impede the hepatic metabolic switch. We found that hepatic expression of several miRNAs including miR-33, miR-20b, miR-34a, and miR-454 was affected by delaying feed consumption for 48 h. For example, we found that delayed feeding resulted in increased miR-20b expression and conversely reduced expression of its target FADS1, an enzyme involved in fatty acid synthesis. Interestingly, the expression of a previously identified miR-20b regulator FOXO3 was also higher in delayed fed chicks. FOXO3 also functions in protection of cells from oxidative stress. Delayed fed chicks also had much higher levels of plasma ketone bodies than their normal fed counterparts. This suggests that delayed fed chicks rely almost exclusively on lipid oxidation for energy production and are likely under higher oxidative stress. Thus, it is possible that FOXO3 may function to both limit lipogenesis as well as to help protect against oxidative stress in peri-hatch chicks until the initiation of feed consumption. This is further supported by evidence that the FOXO3-regulated histone deacetylase (HDAC2) was found to recognize the FASN (involved in fatty acid synthesis) chicken promoter in a yeast one-hybrid assay. Expression of FASN mRNA was lower in delayed fed chicks until feed consumption. The present study demonstrated that many transcriptional and post-transcriptional mechanisms, including miRNA, form a complex interconnected regulatory network that is involved in controlling lipid and glucose molecular pathways during the metabolic transition in peri-hatch chicks.

Highlights

During embryonic development, chicks utilize yolk lipids for energy
We found that several metabolic pathways involved in lipogenesis, lipolysis and carbohydrate metabolism were affected by delaying feeding of male broilers for 48 h
We found that hepatic HMG-CoA reductase mRNA levels were significantly lower in delayed fed chicks until the initiation of feed consumption (Figure 7)

Summary

Introduction

During the last stages of development, the embryo absorbs the yolk sac, which continues to provide a residual lipid source during the first few days post-hatch [1]. Following feed consumption after hatching, the chick’s metabolism must switch to a mainly carbohydrate-based energy source. During embryogenesis, hepatic expression of genes associated with lipid oxidation is high, and post-hatching hepatic lipogenic gene expression increases as feed consumption begins. Glucose levels increase after hatch, resulting from both increased breakdown of hepatic glycogen stores as well as increased glucose. Genes 2019, 10, 272 production from a carbohydrate rich diet [2]. Delayed feeding of chicks for 48 h delays the induction of hepatic lipogeneic gene expression [3]

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