Abstract

BackgroundMaternal riboflavin deficiency (RD) induces embryonic death in poultry. The underlying mechanisms, however, remain to be established and an overview of molecular alterations at the protein level is still lacking. We investigated embryonic hepatic proteome changes induced by maternal RD to explain embryonic death.MethodsA total of 80 45-week-old breeding female ducks were divided into two groups of 40 birds each, and all birds were raised individually for 8 weeks. All the female ducks received either a RD or a riboflavin adequate (control, CON) diet, which supplemented the basal diet with 0 or 10 mg riboflavin /kg of diet respectively.ResultsThe riboflavin concentrations of maternal plasma and egg yolk, as well as egg hatchability declined markedly in the RD group compared to those in the CON group after 2 weeks, and declined further over time. The hepatic proteome of E13 viable embryos from 8-week fertile eggs showed that 223 proteins were upregulated and 366 proteins were downregulated (> 1.5-fold change) in the RD group compared to those in the CON group. Pathway analysis showed that differentially expressed proteins were mainly enriched in the fatty acid beta-oxidation, electron transport chain (ETC), and tricarboxylic acid (TCA) cycle. Specifically, all the proteins involved in the fatty acid beta-oxidation and ETC, as well as six out of seven proteins involved in the TCA cycle, were diminished in the RD group, indicating that these processes could be impaired by RD.ConclusionMaternal RD leads to embryonic death of offspring and is associated with impaired energy generation processes, indicated by a number of downregulated proteins involved in the fatty acid beta-oxidation, ETC, and TCA cycle in the hepatic of duck embryos. These findings contribute to our understanding of the mechanisms of liver metabolic disorders due to maternal RD.

Highlights

  • Riboflavin is an essential precursor of flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD)

  • The beta-oxidation of lipids was severely impaired in riboflavin deficiency (RD) embryos, as indicated by the reduction in the activity of acyl-CoA dehydrogenase, a flavin-dependent enzyme, and the accumulation of lipids and fatty acid oxidation intermediates in the embryonic liver [7, 9]

  • Proteomic analysis revealed that maternal RD mainly affected proteins involved in the tricarboxylic acid (TCA) cycle, fatty acid beta-oxidation, and electron transport chain (ETC) processes, suggesting that these processes are associated with embryonic death

Read more

Summary

Introduction

Riboflavin (vitamin B2) is an essential precursor of flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). An explanation of the sudden death in RD embryos is due to the inhibition of the various critical biological pathways, leading to energy depletion, lipid accumulation in the liver, and severe hypoglycemia [8, 9]. The beta-oxidation of lipids was severely impaired in RD embryos, as indicated by the reduction in the activity of acyl-CoA dehydrogenase, a flavin-dependent enzyme, and the accumulation of lipids and fatty acid oxidation intermediates in the embryonic liver [7, 9]. Cogburn et al (2018) recently confirmed that RD in mid-stage embryos leads to a reduced expression of numerous genes involved in the beta-oxidation of lipids and energy depletion at the transcriptional level, including medium chain acyl-CoA dehydrogenase transcripts [8]. We investigated embryonic hepatic proteome changes induced by maternal RD to explain embryonic death

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call