Maternal diet deficient in riboflavin induces embryonic death associated with alterations in the hepatic proteome of duck embryos

Maternal 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.

Maternal 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.

A 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.

The 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.